Autonomic Nervous System Lecture Notes PDF

. 1. 10/15/2024(Tues) [inaudible background conversations] [student laughs] - [Professor] All right. Everybody able to see slides. No? - [Student] I don't see it. - [Professor] No? - [Student] Maybe it's a very [inaudible] slideshow. [keyboard keys clicking] [inaudible background conversations] - [Professor] No? I shall call. [inaudible background conversations] Hi, I cannot get my computer to work. It switched. Yeah. It was all set up and fine. Then I set it [inaudible]. Yeah, thanks. [inaudible background conversations] All right, technical delay. I swear I didn't touch anything but-- so can't talk about the exam. We still have somebody who hasn't taken it and that won't take it until Friday. That means I will not grade the exam until Friday, and so you'll have to be patient, so sorry. But it looks okay. Anyway, we'll see. [chuckles] So, thanks for those of you showing up after--I mean, weren't we just here? [laughs] Oh, my goodness. We were just here. All right, so I can do interpretive dance. I'll just start chatting here for a second. So I've got--I do have this in front of me. So today, we are starting with autonomic nervous system. And so for the last few weeks, we have been in our sensory system and taking information going into the brain. Yay, she's going to come solve our problems. And so now we're switching to information, essentially going back out. And I'm going to show you that as we look at the autonomic system versus our somatic system. And we'll do a little bit of comparison between those two. And then we'll talk primarily about autonomic outputs. So one of the things that you're going to see with the somatic system--so we just did somatosensory-- so sensory information coming in from the body, and with our somatic system, we have the same sensory input and then motor output. We'll start that motor output piece on the second half of today. With our autonomic system, we have the same kind of setup. You've got sensory information, coming into your autonomic nervous system and then motor output as well. [Professor laughs] I tried switching displays. That didn't do anything. It's very strange. - [Student] Wait, are you trying to, like, get it to PowerPoint? You'll click the bottom thing, like at the bottom. - [Professor] We've-- - [Student] Not that one. Go over to your--this way-- get over somewhere. - [Professor] We've tried. Yeah. We've been doing that. It's a display issue. - [Student] And it's not "use slideshow" at the very top. No, no, no, the-- - [Professor] There you go. Switch displays. - [IT Employee] Yeah, it might have been-- see, it was mirroring your settings. It might have just been a display issue mirroring the wrong thing. - [Professor] Anyway, okay, we're fixed. Yeah, I swapped displays. I mirrored displays. I hit all the buttons. Anyway, we're all fixed up so. Okay, same thing. Objectives for today is just keeping the different aspects of the autonomic nervous system straight. So there's a bit of a structural component to this, there's a functional component to this, and there's a bit of a pharmacology or pharmacological component of this and that we'll talk about each of these. Then that very last piece of this is a reflex. And so we'll talk about what that reflex arc is, and then you can work through an example reflex on your own. I just need you to know that it works by reflexes. And then we'll finally talk about what controls, what are the control centers for our autonomic system, so. To remind us where we are, so today we are peripheral nervous system. So outside of the brain and the spinal cord, so our efferent division and down here with our autonomic nervous system. Despite there's still a sensory component to this that comes in, you don't really see it on here, but when we talk about autonomic control, it is very much an efferent control system. It's like a motor system, but it's autonomic. So, okay, this is what I was trying to talk through, which hopefully, this makes a little bit more sense. When we see an image of this, we were just here with our somatic system and so somatosensory information coming in by sensory neurons. And then later today we'll talk about motor output in our somatic system. But the autonomic, which is what we're talking about first, same thing, you have sensory information coming in. In the case of our autonomic nervous system, we talk about this type of sensory information is coming from interoreceptors. So these are internal, a lot of this is our internal organs and systems. And so controlling glands and organs. So very much internal homeostasis. And so that sensory information is coming from these internal visceral receptors or interoreceptors. As this is a pretty simple concept, not complicated, we leave it at that. So that's sensory information and the type of receptor varies by the type of information that it is. But because the motor system, the outgoing information of your autonomic system is a little more complex, that is what we focus on so. One of the points that I want to make about the autonomic nervous system is this is very much our involuntary branch. So when we talk about somatic motor control, that's typically, we talk a lot about voluntary movement, we'll talk a little bit about involuntary movement, but with our autonomic system, it's very automatic, I think about it that way and in control of these involuntary systems. Okay, but again, so we'll start off comparing that motor system between autonomic and somatic. So this is just to show essentially that these both systems are motor and so they're causing whether it is some sort of contraction in the muscle or movement or secretion, something is motor related. In our somatic system, so this is our skeletal muscle. We have one motor neuron that directly controls that muscle. And so here's that cell body and the spinal cord projects all the way out to that muscle to cause contraction. Talk about that second half of class. With our autonomic system, so in the viscera, it's a two motor neuron series. And so once again, we have that cell body in the spinal cord proper projecting out. And that first neuron here synapsing in something called an autonomic ganglia. We'll definitely define that here. And then that second neuron going from the autonomic ganglion, again, second motor neuron to the effector. And we'll say a lot of things like tissue effector because it could be a gland; it could be an organ. There are a bunch of different autonomic targets, and we'll look at some of those, so. But the big thing to differentiate between our somatic motor system and our autonomic motor system is this basic wiring setup. So somatic is just that single motor neuron coming out of the spinal cord. In our autonomic system, there are two motor neurons in a series. So we'll refer to that first neuron as preganglionic-- and that's because it's before that autonomic ganglion-- and that second neuron as postganglionic. And that's because it's going from the ganglion to the target organ or tissue. A ganglion, just if you need a definition of it, collection of neuronal cell bodies outside of the central nervous system, dedicated to a specific task. So you don't necessarily need to know what ganglion means, but know that there are autonomic ganglion, and we'll talk about a couple different ones. Okay, so emphasizing that two neuron chain, and this is just a different image to reinforce those terms. So here we are, central nervous system, spinal cord, the cell body of that preganglionic fiber, so the first motor neuron in the autonomic nervous system. Synapsing on a second cell. Cell body is in the autonomic ganglion and then projects to that tissue or target organ. So differentiating preganglionic on the front side, postganglionic on the back side. It's just how it's wired; oh, there we go. Central nervous system influence, we'll get to on the end. [chuckles] So. Okay, so now for our autonomic system, it is divided up into two subdivisions. You have your parasympathetic system, and this is your rest-and-digest, as opposed to your sympathetic nervous system, which is your fight-or-flight. And so another key point of our autonomic nervous system is to differentiate how these two very different systems or subdivisions contribute to the control of a lot of our just general bodily functions, from heart rate to digestion, blood pressure, all of these homeostatic activities. So your parasympathetic system dominates in a more relaxed situation. So hopefully, right now, as you're sitting in class, hopefully, not too stressed out, you are relaxed, and so you are in rest-and-digest. And so bodily maintenance type of activities that are occurring. We talk about this as our cranial sacral system, and this is really referring to where the motor neurons emerge from. So you have a collection that emerged from our cranial nerves, and then you have a second collection that are emerging from your sacral, or the base of your spinal cord. And we'll see that on some of these images of our ANS system here in a minute. And then our sympathetic subdivision-- so again, our fight-or-flight-- I like to think about the sympathetic nervous system as sympathizing with my environment. So in cases of high stress, emergency, or where you need to fight or flee is where you are, your sympathetic nervous system is dominant. So this is responses that are preparing your body for some sort of strenuous physical fighting or fleeing. So this is also our thoracolumbar system, and that is reflecting where these motor projections are coming out of our spinal cord. And I steal pictures of-- this is actually, I think, a picture of my former colleague's cat that used to teach on this. So the favorite neuropharm professor at University of Kentucky is where I stole some of these slides from because it's just easy to remember. So parasympathetic, rest-and-digest, you got the cat sleeping; and sympathetic nervous system, and the cat is obviously about to fight or flee, arched back and all of that--probably fight. Again, two neuron chain. The point I want to make: in both systems, you have this two neuron chain. So it's going from your central nervous system where the cell body is in the spinal cord to the autonomic ganglia and then to that effector tissue or organ. All organs receive dual innervation by both the parasympathetic and the sympathetic system. This is actually really beneficial because it's like having an accelerator and a brake, thinking of the sympathetic system as being the accelerator and maybe the parasympathetic system as being the brake. So it gives you a little bit more precise control over these different activities in your body. This is as opposed to your somatic system, so your skeletal muscle system, where you just have an accelerator, you just have go. In your autonomic nervous system, you have go and stop so. So dual innervation and we'll see that in the crazy pictures of the autonomic nervous system. And then of course, the main point that we'll get to visceral reflexes. So your autonomic nervous system is really reflex driven. So it senses something in the viscera and then makes a motor output accordingly. And we'll walk through that. Okay, here's that dreaded picture of the autonomic nervous system. So this is just showing that dual innervation, so parasympathetic here on the right as opposed to sympathetic on the left. And I just want you to see if you look at all the different glands, that you've got both a red and a blue heading in. I have to note, this drives me crazy. This is out of our textbook. Why is parasympathetic red? Shouldn't sympathetic be red? [chuckles] Makes no sense. Anyway, [laughs] I know it's quite silly but I, to me sympathetic, red seems very fight or flee. Yeah, people were not thinking when they made this textbook. So anyway, so we'll walk through all of that. The other thing that you can see in this image, so cranial sacral system, you can see that in our parasympathetic that the nerves are emerging are cranial nerves and then also of our sacral nerves and then the thoracolumbar, all of those projections are, all of the motor output is originating from the thoracic and lumbar sections of the spinal cord. All right, just want to make sure I get all of these points. Okay, another point that we will make repeatedly about the system are these two systems. And our parasympathetic, there we go, in our parasympathetic, you have direct innervation of your target organ. And so that preganglionic neuron is long, heading to that autonomic ganglia, which for the parasympathetic system is very often in the tissue itself. And so that allows for very precise control, specific control, specific innervation of those target organs. And this is as opposed to our sympathetic nervous system where you can see there's a lot of integration and so the, that preganglionic cell in that autonomic ganglion is outside of the target organ. And so you have diffuse innervation, coordinated innervation in your sympathetic system. And this will little, make a little bit more sense when we talk about the coordinated activation of our sympathetic system. All right. - [Student] What's this you said in the tissue itself? - [Professor] In the case of our parasympathetic nervous system, the autonomic ganglia is in the tissue itself. And I'll repeat this again as we talk about each of these systems individually. Okay, so lots of words on this slide, and it's just to go with this image that I stole from my old textbook. I really like it because it shows you, without the sympathetic system, the specific innervation from our cranial versus sacral system. So this is all parasympathetic that we're talking about now. So cranial-sacral outflow. Preganglionic parasympathetic neurons, so meaning that first neuron-- first motor neuron in the chain--are cranial nerve nuclei or the sacral spinal cord projections. So, again, cranial sacral system. So it's using the cranial nerves for these motor neurons. And this reminds me, I should make a quick point for our cranial nerves. They carry both sensory information and motor information. So it's okay if you're sitting here thinking, "Didn't we just talk about this with sensation?" Yes, it's because those cranial nerves carry tracts that go in both directions. It's just kind of like either side. You know, those tracts have bundles within them, and so sometimes that information is coming in, and sometimes that information is headed out. It just depends on what portion of the bundle within that tract that that information is, so. So for our parasympathetic nervous system, a couple of these key preganglionic nerves are cranial nerves III, VII, IX, and X. So oculomotor nerve (Number III). So cranial nerve Number 3, this is going to ciliary muscles of our eye, that pupil sphincter muscle. So I think I warned you about this when we talked about the eye, that there was autonomic innervation of the pupil. We'll talk about that again. And so, yep, so you can see that projecting here. Facial nerve, so cranial nerve Number 7, goes to submandibular and sublingual salivary glands for salivation, lacrimal, which is tear ducts, and nasal glands. So what else did we talk about for cranial nerve Number 7? Taste, yep. It's one of the taste. And so this makes sense that you've got motor information from your parasympathetic system heading to some of these same regions. So you can control salivation in the mouth. Glossopharyngeal, so Number 9. Parotid glands, so more salivary glands, and vagus. So there's an entire organization in the Society for Neuroscience that met just last week called Club Vagus. So they all study parasympathetic nervous system. This always cracks me up. Maybe you guys will remember it for that. I'm not a member of Club Vagus. Seems very cool. It carries--so the vagus nerve is your primary parasympathetic nerve. And so your vagus nerve carries 75% of your parasympathetic tracts to your body. And so if we follow this, and so this is that bottom green line here, so there's that X for vagus, it is headed down to our heart, to our stomach, to our colon, our intestine. So just very broad control of our thoracic and abdominal organs. Again, all controlled by our vagus nerve. So very key, key parasympathetic cranial nerve. All right, so now moving down to the sacral portion of our spinal cord. And so this is S2 through S4; there's even a little S1. So and again, that very base portion of the spinal cord that we talked about, you have nerves that project to pelvic ganglia located in the bladder, ureters, descending colon, rectum, and reproductive organs. And so this is that, again, bottom portion, essentially that tail-end--without being the tailbone-- portion of your spinal cord. And so you can see those projections. Just remember cranial, sacral, and think about the logical things that come off of the cranial versus sacral system. I think vagus, just remember that vagus is the one that is heading down into your heart, your stomach, and your colon, and, again, vast majority of your organs under parasympathetic control comes through that-- that vagus nerve. Making this point again. So that preganglionic neuron is quite long and that postganglionic neuron is quite short and that's because that autonomic ganglia is near or within the wall of that effector tissue or organ. And so we'll see that, we have a couple comparison images at the end. There's a couple tables at the end that also make that point. And again, this is because we have that very specific innervation with our parasympathetic system. But that's a good thing. You want specific innervation of your heart. So control of the heart, of heart rate and contraction. You absolutely want very specific control of that. Most of these postganglionic neurons, these very short tiny neurons are passing uninterrupted again directly to the target organ. Honestly, that is also, that applies to the preganglionic. So the preganglionic heading on out to that target organ to that autonomic ganglia, which is within that organ or tissue itself. So specific innervation. So parasympathetic responses, again, remember our relaxed chilled out cat. So these are all of the actions of our parasympathetic system. So in the eye, that is pupil constriction, lens accommodation. Does anybody remember what lens accommodation is? Focusing? Yep, your ability to focus down on your, your iPad or your computer, that's accommodation. Constriction of the pupil also under autonomic control as one of our parasympathetic responses. So tear gland, lacrimal glands, tear glands secretion, salivary gland secretion, so this is promoting digestive related activities. rest-and-digest. GI tract, so all the things that you learned about with Dr. DeMorrow under parasympathetic conditions, it is promoting secretion, peristalsis, sphincter relaxation. So digestion related activities. Heart rate, it decreases your heart rate, decrease, I'll just leave it at decreases heart rate. Bladder, detrusor contraction and so this is for urination and also internal sphincter relaxation. So promoting urination. And then in our lungs, the bronchi and bronchioles, constriction under rest-and-digest. So how do I remember all of this? Your parasympathetic nervous system, and this, I got this from my former postdoc that used to teach this SLUDD, so salivation, lacrimation, urination, digestion, defecation and the three decreases. Does anybody else have a better way to remember what the parasympathetic responses are? Is there some other, I think he got this right out of a med school, I don't know. - [Student] I've heard point and shoot, like, when you're urinating for pee, point and shoot. - [Professor] Okay, there you go. [laughs] Whatever works to help you remember all of these parasympathetic responses. And this just comes up, you know, I might ask a question about what controls urination? Is it the parasympathetic system or the sympathetic system? And so just think about things that occur during rest-and-digest or remember SLUDD and three decreases or whatever mnemonic works for you. Okay, any questions on the parasympathetic system? All righty. So sympathetic. So a couple key things about our sympathetic, again, it's sympathizing with the environment. This is our fight-or-flight system. So preganglionic neurons, this is our thoracolumbar output. And so those preganglionic neurons are in the thoracic to lumbar section, so right here in the middle. Bilateral, across spinal segments. Thoracic one to lumbar two is just what they're trying to show all the way down here. And this includes splanchnic nerves, heading out to a celiac ganglion or hypogastric ganglion down here. Again, these are the preganglionic. These are the first motor neurons in the line. In this case, our thoracolumbar system, if you will notice, seems very-- I guess you could say intertwined. And that intertwining of all of these, that diffuse innervation, is what contributes to how this system functions, which is--we'll essentially show in a couple slides here. So the postganglionic neurons, so coming off of the autonomic ganglion, and so we have autonomic ganglion that are typically outside of the target organ. So celiac, hypogastric down here, and we do still have a couple coming off the top here. Also, the sympathetic chain ganglia. All of these are autonomic ganglia that are outside of the target organ. So characteristic of our sympathetic system is-- the autonomic ganglia is typically outside of the target. So those postganglionic neurons then arising from the autonomic ganglion. In the case of our sympathetic chain, these innervate smooth muscles that are part of our blood vessels, piloerector muscles, and sweat glands, also innervate cardiac muscles, smooth muscle of the bronchi and the iris. And so we can see that up here, coming off that sympathetic chain ganglia. So this is about 8% of your nerve fibers within those spinal nerves. I do want to point out, the little dashed line here is actually feeding back into the spinal cord. And so if you--we don't do it for this class, but if you ever talk about the autonomic system in depth, there's a lot of this almost circular innervation across especially the sympathetic chain ganglia that runs the length of your thoracic down to the top of your lumbar part of your spinal cord. So this is all very integrated, all intertwined, and essentially when you set off one portion of it, you're going to set off the entire portion of it. And we'll talk about that in a couple slides. Okay, so things that we call these prevertebral ganglions, so that celiac ganglion here, so heading out to our stomach, our adrenals, our kidneys, and our ureter. And that hypogastric below the gastric plexus, another, and you can see this is heading on out to the bladder. And then finally, one of our major autonomic ganglion is that adrenal medulla. And so we'll put that on the next slide. So our adrenal medulla is one of our key areas, and it is the area for the projection of epinephrine. So we're going to talk a little bit about-- we're talking both about how this is wired in as part of our sympathetic nervous system, but we'll also talk about a little bit of pharmacology with our adrenergic signaling. So preganglionic sympathetic axons synapse on cells of the adrenal medulla. And so that's what this is trying to show you. And so here's the spinal cord. Here's those cell bodies. Here is that first cell, so preganglionic, sympathetic preganglionic, innervating that adrenal medulla as--it's an autonomic ganglia. And then our adrenal medulla releases neurotransmitter, norepinephrine or epinephrine, as a hormone. So it releases both norepinephrine and epinephrine into our bloodstream. And then epinephrine and norepinephrine can go to the target organs via the bloodstream. Yep. - [Student] I'm sorry, when we're sorting back to the pre and post ganglia, are they like specified by that name like a-- that relationship just based on their proximity and network? - [Professor] Yeah, that especially for us, so. The main point here is that the postganglionic neurons in our sympathetic nervous system are coming off of these autonomic ganglia that are outside of the target organ. So, distant. Okay, so back to the adrenal medulla. And so here on the left, just standard, essentially standard sympathetic signaling outside of the adrenal. And so here is a an autonomic ganglion. And so preganglionic fiber synapses onto the second fiber within the autonomic ganglion that projects out to some target organ, but for our adrenal medulla, so we have preganglionic neuron projecting to the adrenal medulla and then the adrenal medulla releases epinephrine and norepinephrine into the bloodstream. So hormone-based signaling, this is actually, gives it a couple of key effects. So this means that adrenaline and epinephrine, same thing, or norepinephrine can reach really distant sites in the body by, through our vascular system. Again, not very specific, it's dumping all that epinephrine into your blood system. And so it can go to every point in the body that your vasculature is reaching and brain for that matter. And that's what that image is trying to show. So it's reaching all of that through your blood circulatory system. The other key thing about this is that the breakdown of norepinephrine and epinephrine is much slower. And we'll talk about the things that break it down in a couple slides, but because it is in the blood system, it just takes it a little bit longer to get that broken down. And the mechanism of breakdown's just a little slower. Key other factoids about this, I'll start up here. So about 80% of that hormone release from your adrenal medulla is epinephrine and then about 20% is norepinephrine, working through, see yeah. So the great thing about this ability to stimulate structures of the body that are not innervated directly by sympathetic fibers, and that's because it's dumping epinephrine and norepinephrine into your circulatory system and it gets to those diffuse target sites by your blood system. Questions on that? Okay. Oh, almost forgot. Chromaffin cells are what synthesize epinephrine. So that's a great little factoid and term that always pops up in a number of places. Just remember, chromaffin cells are what are synthesizing that epinephrine. And we'll talk about that in a couple more slides. Okay, sympathetic responses. Again, this thinking about sympathizing with your environment, I think this is a little bit easier to remember. So any kind of physiological activity that is going to prepare you to fight or flee. So dilates your pupils, increases your heart rate, increases contraction of your heart, it makes your, essentially your salivary glands become more viscous, so less secretion, thicker, relaxes the bronchials and bronchi, secretes sweat. In vascular smooth muscle, you get, oh, it looks like I didn't specify, you get some contraction relaxation depending on what it is. GI tract inhibits secretion, inhibits motility, and it contracts sphincters. So it essentially shuts down digestion. You don't want your body to be trying to digest when you're trying to fight or flee. And so I think some of this makes a lot of logical sense. And same for your bladder. It is essentially shutting down urination so that you can focus on activities that you need to fight or flee, like raising your heart rate, increasing contraction of the heart. So one of the key characteristics of this sympathetic nervous system-- and this is based on how it's all interconnected and intertwined in its connections across that sympathetic chain ganglia-- is that you get something called mass discharge. So as I already hinted, once you essentially activate a portion of that sympathetic chain ganglia, the whole thing is getting activated. So you get mass discharge of your sympathetic nervous system. It discharges simultaneously as a complete unit. So this is typically initiated by your hypothalamus. Remember your hypothalamus, your homeostasis control center up in your brain. So your hypothalamus is one of your key control centers for your sympathetic-- or, for your autonomic system in general. And so something that is going to set off a mass discharge is typically initiated by that hypothalamus. So in response to fear, severe pain, or rage, you're going to set this off. And maybe you have felt this, have you felt an adrenaline rush? Yeah, I know I have. Certain situations. And that adrenaline rush that you feel is that mass discharge of your sympathetic nervous system. So in that case, so the same things we just talked about in this slide, all of these sympathetic responses. So arterial pressure, increase, blood flow, depends on where you're at. Increase in cardiac and skeletal muscles, decreases in your skin and viscera, increases cell metabolism, increase blood glucose concentration, essentially increasing all the things that you need to fight or flee, so. All right. And shutting down things like GI tract or urination because you don't need to be doing that if you're trying to fight or flee. So think about that logically. Think about the things that you need in your body, especially heart rate. You need that heart rate up. You need that contraction up. You need that blood flow to your cardiac and skeletal muscles and so that you can fight or that you can flee. Okay. Questions about the physiology portion of parasympathetic rest-and-digest, sympathetic fight-or-flight. Yes. - [Student] Sorry, so back to the adrenal medulla, when you were talking about how they stimulate structures not directly innervated, on that like table of the mass discharge, are some of the examples like stuff that's stimulated by the adrenal medulla, or? - [Professor] Absolutely. - [Student] Okay. - [Professor] Yes. Yep. In fact, so that's the great thing about the sympathetic system, too. Not only do you have that mass discharge of the sympathetic chain ganglia, but you also have the stimulation of the adrenal medulla and then the adrenal medulla releasing it into the bloodstream. It's a little bit slower, but it lasts much longer. And so I don't know if you can--if you've ever-- if you can detect it, that adrenaline rush that you physically feel. It's a little delayed from whatever event is going on. And sometimes you can have it happen, you can have an adrenaline rush like happen when you don't intend to. And it just makes you realize because it's got to be released into the circulatory system, that's a little bit slower to get to the rest of your body. And so sometimes you may-- and maybe the next time this happens to you, you'll be like, "Oh, yeah, that was really delayed." And it's because of having to release it into your blood like a hormone, hormone-based signaling. Great question. All right. Any other questions about the physiology piece? Okay. Time for some pharmacology. Yay! That's why we're all here; right? Okay, so autonomic neurotransmitters are actually pretty logical. I like this. I don't know how old this image is. It hasn't changed. I like it because it's something that I could draw if I had to, and it really helps me make sense of all the neurotransmitters involved. And so there's, and I say that, and there's really just two that we were--I guess three. So we have acetylcholine, ACh, and then of course, we have our norepinephrine and epinephrine. And so you can see that. Keeping track of what projections are, what is the hard part. And so we summarized this here in our or overall, all preganglionic fibers are cholinergic. So remember it's all preganglionic fibers are cholinergic as we're going to learn about in the second half of class. Our skeletal muscles also use acetylcholine for contraction. So this is a motor system and so it makes sense that it's using acetylcholine to drive some motor activity. So all preganglionic are acetylcholine. You'll see that there are N, these are all nicotinic receptors. And so these are all ligand-gated ion channels for this, for the nicotinic receptors. Then our postganglionic fibers in the parasympathetic system. So this is up here in the top. These are also cholinergic, oh, I didn't circle those too so that you can see those are cholinergic. But these are the muscarinic subtype. So these are G-protein-coupled receptors. So this is on smooth muscle, some glands in your cardiac muscles. Again, remember your direct innervation of our parasympathetic system and this image is great. It shows that, so you have that. In your parasympathetic, you have that long preganglionic fiber and then your autonomic ganglia likely within the tissue itself or very close by. And so short postganglionic fiber, also cholinergic. So parasympathetic is all cholinergic. Then in our sympathetic system, the postganglionic fibers are mostly adrenergic. So here's post ganglionic second in line. So norepinephrine acting on having receptors, alpha one, alpha two, beta one or beta two. You also have postganglionic receptors that are, I should say postganglionic signaling that is cholinergic in your sweat glands. And so I remember this one exception is that my sweat gland is cholinergic, it's a muscarinic receptor. And then down in our adrenal medulla, again, of course, when the adrenal medulla releases epinephrine or norepinephrine, that is into our bloodstream and it's going to adrenergic receptors that are diffusely scattered across our body. Okay, so just a little bit of reminder on this. For adrenergic neurotransmission, that ligand is epinephrine, adrenaline, or norepinephrine. It can be excitatory or inhibitory depending on the receptor that is present. We'll show that real fast. Receptors can respond to autonomic nervous system neurotransmitter or to adrenaline released from that adrenal medulla into the bloodstream. Most sympathetic postganglionic cells, again, those effectors are innervated by your sympathetic division and the sympathetic stimulations are more widespread. They're widespread, we talk about that because of that adrenal medulla secreting epinephrine and norepinephrine into the bloodstream and going all over the body. So very widespread. Sympathetic reactions are also longer lasting because that transmitter is not directly broken down but tends to diffuse away. And the mechanisms that we have in place to inactivate it, catechol-O-methyltransferase, which is on the next slide or monoamine oxidase just physically take longer to break down the epinephrine or epinephrine and norepinephrine. So this is straight out of your slide on neurotransmitters. Just to remind you that adrenergic receptors are all G-protein-coupled receptors. We have alpha receptors, a1, generally excitatory; a2, generally inhibitory. Beta receptors, generally excitatory, b1; b2, generally inhibitory; b3 is only on your adipose tissue. Activity of our norepinephrine or epinephrine terminated in one or two ways, can be taken back up by a neuron that released it or it gets enzymatically inactivated again by that catechol-O-methyltransferase or COMT or monoamine oxidase. Last slide for this first session. So summary of those sympathetic functions in all the receptors involved. So great news for this class. This is not a pharmacology class. You do not have to memorize any of this. Just know that your sweat glands are cholinergic and that everything else is adrenergic. So don't have to memorize it for this class. But this is coming, and this is some of the most hated stuff in the cardiac system. Sorry, [chuckles] that's where I pass it off to below the neck. All right. I will stop here for now, and we'll pick back up at 10. [inaudible background conversations] Almost finished. [chuckles] Hey. What's up? - [Student] So I know that with parasympathetic [inaudible] does that mean that it's like, I guess like they're inhibitory because of it is parasympathetic, or does it just depend on-- - [Professor] Yeah, it depends on what the receptor is on the department. - [Student] Okay, okay, well, thank you. Thank you. - [Professor] But [inaudible] we think about it as generally kind of inhibitory because it's a relaxed-- - [Student] Yeah. - [Professor] [inaudible] - [Student] That's what I was insinuating- - [Student] Oh, I'm so sorry. - [Student] No. [inaudible background conversations] [paper rustling] [paper thuds] [inaudible background conversations] [inaudible background conversations] - [Student] Okay, we have a question. - [Professor] Yeah. - [Student] So, when does the adrenal medulla releasing hormones? Is that like-- - [Student] Is that active? - [Professor] So this is all very coordinated, and so you set off that sympathetic chain ganglia, and it starts to stimulate your adrenal medulla, too. It's all very coordinated. - [Student] So like everything in the sympathetic? - [Professor] Yes. - [Student] It uses the adrenal medulla, everything? - [Professor] Well, no, not-- not everything uses the adrenal medulla, but it--because it releases into the bloodstream, it is getting to a wide variety of places. - [Student] Okay. - [Student] So is it like when you have an adrenaline rush? - [Professor] Yeah. - [Student] Is that what it is? It's used-- - [Professor] Yeah. - [Student] Okay. - [Professor] That adrenaline rush that you feel is in your circulatory system-- - [Student] So that's why it's so late-- - [Professor] But if you felt it-- - [Student] Okay. - [Professor] You feel it all over your body. Right? - [Student] So-- - [Professor] As I'm sitting and thinking, I feel--I always feel it in my arms. I feel that rush. - [Student] Yeah. - [Professor] That rush is your adrenal medulla releasing into your bloodstream. - [Student] Okay, so it's just because sympathetic, it's like being active doesn't happens, when you say the adrenal medulla? [student chuckles] - [Professor] It is all very coordinated. - [Student] Okay. - [Professor] And it all mass discharges-- - [Student] [inaudible] - [Student] Basically, like it depends on what's the theme-- what's the theme is; right? - [Professor] Because they're all interconnected, and so this, when you activate this, you activate a lot of stuff, because you need-- they also talk about it as sympathetic tone. And so I think if you are a high sympathetic tone, you're not necessarily setting off your adrenal medulla, but I didn't get that out of the textbook. - [Student] Okay. - [Professor] It's out that, like discussion. - [Student] Okay. - [Professor] Maybe that's what you're asking. - [Student] Yeah. - [Student] Okay. - [Professor] That's kind of like, yeah, that's kind of what we were asking. Yeah. - [Student] Okay. - [Professor] Yeah, and it, yeah, because it doesn't necessarily talk about that in the textbook. It just really compartmentalizes this if it makes sense, you know what I mean? It's what I'm saying. - [Student] Okay. - [Professor] You can have-- we have a higher tone but maybe it doesn't set off the mass discharge. I think some part of that is more the, less activity of your parasympathetic, not so much the activity. I think this is-- - [Student] Yeah. - [Student] I mean, it's like the end of- - [Student] Okay. - [Professor] Yeah. - [Student] Gotcha. Thank you. - [Student] Thank you. [Professor faintly speaking] [inaudible background conversations] [inaudible background conversations] - [Professor] Yes. - [Student] Are you saying that norepinephrine gets regarded to adrenal medulla? - [Professor] Yeah. [student faintly speaking] - [Professor] Yeah. - [Student] Okay. [inaudible] [inaudible] - [Professor] Yeah. [inaudible] [student faintly speaking] - [Professor] Yes, yes. [inaudible] - [Student] That's good. [inaudible] - [Professor] The two systems are like having more-- So the parasympathetic [inaudible] - [Student] So is it always-- - [Professor] More, having more-- Yeah. [inaudible] - [Student] I just thought it makes sense because, like, it's like resting, you turn into-- - [Professor] Oh, like, but yeah. And this is a very general-- because sometimes we go back to activate something [inaudible]-- - [Student] Right, that's why it is like you're talking about like, you know, the GI tract, like the vagus stuff, like turning off [inaudible] - [Professor] [inaudible] - [Student] So it's just a general--[faintly speaking] So in this case, we're activating these-- - [Professor] Yeah, it's like [inaudible]. Yeah. - [Student] To shut it down. - [Professor] Yeah. - [Student] So it's like a double-- - [Professor] Well, yeah, it is. In the case of this-- [inaudible] It turn into contraction. So that is your, you are activating. - [Student] Activating [inaudible] [Professor laughs] - [Professor] Well, in that case, [inaudible] the sphincter, sphincters [inaudible] [inaudible] [student faintly speaking] - [Professor] Yeah, okay, so that'll open it. Relaxation. [faintly speaking] [inaudible] - [Professor] Oh, yes. I may be getting the same question. [inaudible background conversations] Yeah. [student faintly speaking] Okay. - [Student] So but on the same [inaudible] [Professor laughs] - [Professor] Yeah. - [Student] But, yeah, I just read about [inaudible] - [Professor] Yup. Somebody always has something [inaudible] [inaudible background conversations] [inaudible background conversations] [inaudible background conversations] [inaudible background conversations] [inaudible background conversations] [inaudible background conversations] - [Professor] Okay. Welcome back. I got some great questions during the break, so I can help, hopefully, try to specify a little bit. So we were actually just talking about this particular slide. So keep in mind that this first dot here is the cell body that's located in the spinal cord. Even though it's in the spinal cord, this is all your peripheral nervous system. This is just where we've drawn the line. And that's because all of these axons heading out of the spinal cord through our spinal nerves, we talk about those as-- those are peripheral nervous system. So that's just where we've drawn the line. The second dot are autonomic ganglia, and that's because the cell body of that postganglionic cell is in that autonomic ganglia and that the adrenal medulla is one of those autonomic ganglia. Second clarification, let me go back to-- so we talk very generally about parasympathetic as being rest-and-digest, and some folks started to say, "Oh, this is all inhibitory." You have to be careful with that. Even though we are resting and digesting, there are activities that you have to activate to digest. So you are activating muscles or your enteric nervous system to digest. And so there are things that are, you know, being activated within digest. So don't-- even though this seems very inhibitory, there's a lot of action happening to rest-and-digest. Does that make sense? Because I think some of you might have been trying to say, "oh, this is inhibitory," and there's both inhibitory and excitatory action happening in order to elicit resting and digesting. And then, of course, sympathetic, all very activating. But the action of the neurotransmitter is always dependent upon what receptor is present. And we are not--thankful, we're not a pharmacology class. And so we punt this to a therapeutics class. We just set up what the neurotransmitters are, we set up what the two different systems are, and that's all we need to know for this class. Okay. Questions? I have a couple more things that we'll talk about relative to this, any questions? Yes. - [Student] So for the enzymatic inactivators of like adrenergic receptors, do you want us--let's say, like if you have a blank, like a fill-in-the-blank, do you want us to be able to like say like the whole thing, or are you okay with just like COMT and MAO? - [Professor] COMT and MAO are absolutely fine. So no worries. And we will reinforce these two terms a number of times as we get to pathophysiology over the next couple weeks. So this is just the first time you see them for adrenergic signaling. So, okay, and so this is a great-- let me step back for a second. I realize I forgot to say. So synthesis of norepinephrine, we don't have to know a lot of details about it for this class, again, we're not a pharmacology class, but dopamine gets converted into norepinephrine. This can happen in your brain, it can happen elsewhere. And then that norepinephrine gets converted into epinephrine in your chromaffin cells of your adrenal medulla. And I just wanted to make that specific and clear if it hadn't been so. So that's where that comes from. And again, the action of norepinephrine or epinephrine is completely dependent upon which receptors are present and, of course, where those receptors are, what organs they're on. And then we talked about how the epinephrine or norepinephrine can be terminated. Its actions are terminated, they either get taken back up by the neuron that released it, especially if you're in the nervous system, central nervous system proper. Or it can be enzymatically inactivated by either catechol-O-methyltransferase or COMT or monoamine oxidase, MAO. Okay, are we ready to move to reflexes? Maybe not, [laughs] but we are anyway. Okay, so your autonomic nervous system functions through autonomic reflexes. So as it says on the top, ANS maintains visceral homeostasis through these reflexes. So I just wanted to go through a reflex arc because we're going to talk about this with all of our motor systems. So a reflex arc requires you to sense information by sensory receptors. So you have a sensory receptor, some stimulus acting on sensory receptor in your viscera, enteroreceptors are the receptors in your viscera that sensory neuron projects on into your spinal cord. It can project on up to a variety of integration centers, whether it is in the dorsal horn or the spinal cord itself. It will also project on up into your central nervous system and tell your brain what's going on. But the reflex itself is handled at this level of the spinal cord. So sensory information comes in and then it synapses on a couple interneurons and eventually on the motor neuron. So that motor neuron for autonomic system is that two neuron chain. And so we've got a preganglionic neuron and then a postganglionic neuron. Oh, and this is a great picture of that sympathetic chain ganglia kind of up close where you can see that you've got all these circular-like ramifications that they talk about that helps with the integration of that entire sympathetic chain that runs from T1 down to L2. So that motor neuron system, two motor neuron system is what's used to create that visceral effect in the organ or tissue. So you sense it, you send it to the motor neuron, the two motor neuron chain, that two motor neuron chain causes some sort of action. So that's the reflex. This occurs for blood pressure, salivating, your gastric secretions, defecations, gallbladder, pancreas, urination, sweating and blood glucose. These are all autonomic reflexes and, again, just an FYI. So all of those systems that you saw essentially connected by your parasympathetic but also your sympathetic all function through these reflexes. So how do you put this all together? And so this is just an example. I am not going to ask anything beyond autonomic-- your autonomic nervous system functions through these visceral reflexes. And so this is just an example that I want you to work through to really see how this is a reflex. And so we can look at this. So this is autonomic control of blood pressure through our baroreceptors. And so a baroreceptor-based reflex. You can see, you know all these different activities. It has both sympathetic nervous system and parasympathetic nervous system and how both effects happen. Remember, you've got essentially an accelerator and a brake and how that change in the blood pressure then gets communicated back in a feedback loop. So if we work through this, and I'm just going to do this really quickly because you should just go through this and appreciate this at home. So, blood pressure's too high. That activates your baroreceptors and your carotids and aorta; that stimulates, of course, when you're activating those baroreceptors, they're sensory neurons, and so it's going to send that information into your cardiovascular control center in your medulla. The medulla is essentially the home-- so this is in your brainstem-- the home for these autonomic reflexes. And so that then sets off actions in both your sympathetic and parasympathetic. So sympathetic is going to be somewhat inhibited while your parasympathetic is going to be more activated, then that's looking at those arrows. And then you can just kind of trace your way down to what increased blood pressure does for not only the heart rate but also contraction, force of contraction. And that all comes together to reduce that blood pressure and then hopefully feed back to those baroreceptors. So just work through that and think about, the points I want to make is that both sympathetic and parasympathetic have activities, and they're both connected to various tissues to have that reflex effect. Okay. Now you can control at higher levels of your central nervous system how that autonomic system functions. And there are--we're going to talk about four different places, higher centers of autonomic control. So the first up here in our cerebrum or really the limbic system. And that's the point that your thoughts or emotions can influence autonomic function. But this all goes down through the hypothalamus. So via hypothalamus. That hypothalamus is your main autonomic control center. Remember, hypothalamus is our homeostasis center, and you have all these different nuclei dedicated to monitoring blood pressure, body temperature, feeding, digestion, et cetera. A lot of these same activities of your parasympathetic, your rest-and-digest system. So your hypothalamus, when it determines something is awry, can directly initiate autonomic responses through direct projections down to those preganglionic neurons. So that first motor neuron that starts in the spinal cord. So it regulates autonomic responses through projections to autonomic center and regulates through autonomic centers throughout the brainstem as well. So hypothalamus projects straight to the spinal cord to those preganglionic neurons, but also projects to our autonomic reflex center in the brainstem, so in the medulla. And then spinal cord also has a couple reflex centers for urination, defecation and reproductive behaviors. And of course, these are the sacral activities. So in the base of your spinal cord, that is your reflex center, essentially for things that are down on the, you know, lower half of your body. So, but again, main point of this is you can control autonomic activity primarily through your hypothalamus and its projections into the autonomic system. All right, so this is the slide that I stole from my former colleague. Just summarizing our parasympathetic versus sympathetic and some of the key points that we made along the way today. So oversimplified function, rest-and-digest versus fight-or-flight. Neurotransmitter, it's cholinergic for parasympathetic, sympathetic involves our adrenergic signaling with epinephrine and norepinephrine. Preganglionic, craniosacral versus thoracolumbar. Location of the ganglia. And then of course this, essentially the size of the preganglionic versus the postganglionic neurons. Connectivity, specific versus ramified. Ramified, just meaning very interconnected. Regulation of those end organs, very specific and independent in our parasympathetic system whereas our sympathetic was very coordinated. Oh, and one quick last point, parasympathetic, your stat system is essential for life. It's controlling heart rate, blood pressure, digestion, all of these, breathing, all of these activities that are essential for you to live. Sympathetic, not so much, just coordinating that fight-or-flight response. Okay, questions on autonomic. Great summary slide. If you can understand all these points in this summary slide, you've got it. And also add in there the neurotransmitters. Yep. - [Student] What did you say ramified meant again? - [Professor] Just interconnected. And it's just referring back to this, we didn't look very close up. I got this out of a different text at how these, what they call them ramifications of these circular interconnections down that sympathetic chain ganglia. That sympathetic chain ganglia that runs from the top of your chest to the bottom is all interconnected. That's why if you set that off in a sympathetic mass discharge, that whole thing is shooting off. It's all interconnected. All right, let's talk about somatic nervous system. Okay, so change of topic. Autonomic, really one of the, it's not hard, it's just a little detailed. And especially you guys will use that probably more when you talk about cardiac function than anything else. The neuroscientists, it's funny, we just kind of discard it. In fact, I think I made it, I think I made it all the way through graduate school without ever having a class on the autonomic system. Hopefully that helps you guys because that means I've had to absolutely make sense of it myself in order to talk about it. Anyway, but motor system, hopefully, more interesting. So same thing, we've got a few more objectives in this and it's just 'cause motor control has a few more things that we'd talk about. We'll get into a little bit of pathophysiology today, just to go a few basics. And it made me realize, this week is the last of our physiology. Next week we start the fun, the patho. So what I've been waiting for and what you guys have been waiting for. I'm super excited. Okay, so now we're going to talk about movement and there's a couple different types of movement. We have voluntary movement and you'll see that your cortex, your cerebellum and your basal ganglia are very much involved in voluntary movement. We have involuntary movement. And so this is mostly spinal cord-driven, reflexive activity. And of course, we just talked about involuntary visceral motor control with our autonomic system. But this is involuntary somatic motor control, or skeletal muscles. And there are also rhythmic motor patterns. And these are specific patterns of activities. They're often repetitive. There's a lot of stereotypic activities for, you know, particular species. So things like running, walking, chewing, these are all rhythmic patterns that get stored in your brainstem or your spinal cord. And so essentially, some thought stimulates these pattern centers and sets them off. And so walking is a great example, as I realize I'm standing here walking and pacing as I talk. It's my brain just apparently told my walking center to walk, and so therefore I'm walking. But we are not going to cover the rhythmic motor patterns in this class. We're going to just stick to our voluntary movement. And then we'll have a little bit of involuntary tomorrow on Thursday when we talk about reflexes. So just a reminder of where we are. So now we are output from the central nervous system to our periphery. So we were just here in blue, and now we're taking this green again, still all efferent, still all peripheral nervous system, but now moving towards motor neurons. And then on Thursday we'll talk about-- we'll finish off movement and then talk about skeletal muscles. So the whole reason that I did autonomic first is so that we can work all the way from brain to spinal cord to skeletal muscle to understand how motor control and movement works. Just a quick highlight. So all of those different brain regions that we talked about when we did that gross neuroanatomy, look at how many of them are involved in motor control. And so we will talk about the role of all of these different regions in movement, whether voluntary or involuntary. Okay, so starting off with voluntary movement. So this is you choosing to move, having a thought of "I need to move" or reacting to some stimulus by thought that you need to move. This is purposeful, this is goal-directed voluntary movement. So there are three major regions of the brain involved in central nervous system control of voluntary movement. Cerebral cortex, and then we'll talk about a bunch of different regions that are-- have specific roles, your basal ganglia, and we'll talk about the structure of the basal ganglia. And then we will, hopefully, we'll just start to touch on if we get to it today. My hope was to get to that to cover it today but also on Thursday because it's a little complex, but it's necessary for pathophys next week. So we've got to understand how the basal ganglia works. And then cerebellum. So cerebellum being your timing and coordination center for motor control. Remember that cerebellum's tucked up underneath the occipital lobe. So vision's here, and then cerebellum right underneath it. And we have a couple other roles. So I just showed you the table with all these different brain regions. And so we have a couple other regions with smaller roles, involuntary movement. So we'll talk about the red nucleus, reticular formation, our arousal center and how it's involved, our pons and the brainstem, and, of course, our thalamus. So we are going to start with cerebral cortex. So starting at the top and working down. Just to show you an image that you've seen before with all of the sensory systems that we have talked about. I want you to be able to appreciate where that primary motor cortex is with respect to our sensory systems. And so here is that primary somatosensory cortex on the posterior backside of that central sulcus So remember that central sulcus kind of runs down the middle of the side of your head, and it's just a deep valley between those two kind of pieces of cortical tissue. And so just opposite, on the opposite side of that valley, that central sulcus, is the primary motor cortex. And so we're going to talk about how that primary motor cortex and its specific innervation to our spinal cord motor neurons and how it directs a lot of our fine motor control. But you also see that we have what is kind of a secondary movement motor control area. This is made up of our premotor cortex and supplemental cortex. So up here just in front, this is all in the frontal lobe. So your somatosensory cortex was in parietal and then your motor cortices, all three of them are in the frontal lobe. And of course, we've got your speech center located just underneath the supplemental motor cortex. Okay, so to orient you to this kind of crazy picture, I like this because it really shows everything, but I don't like this because, so this is supposed to be the other hemisphere. So you have two hemispheres here, just looks kind of funny. So it's trying to show you a view, kind of sorted down from the top inside where you see that there are two hemispheres and that's just to make the point that your motor cortices are present in both hemispheres of your brain and same for your somatosensory areas as well. So primary somatosensory cortex, again, right there behind that central sulcus, you have the primary somatosensory and then your somatic association area. And so that integrates multiple sensory information and it really starts to coordinate with your movement centers and we'll talk about that essentially the flow of information to perceive something and then affect a movement. So, okay, so motor cortices. So we have three primary motor cortices that we'll talk about. Or I should have said three main ones because the first or the second, last one we'll talk about is the primary motor cortex. So three motor cortices. They each have roles in voluntary movement and very specific roles in voluntary movement. So first off is this premotor cortex. There we go, so premotor, actually that's the one down here at the bottom. And so it is adjacent to the face and the mouth portion of the primary motor. The premotor is involved in your mental planning and staging of movement. So it's essentially making a motor plan and it makes that plan in the anterior portion. So the anterior part or the frontal part of the premotor area, forms this motor image. What does it look, what do all the movements look like from the brain perspective? And then the posterior portion here, is what translates that and then sends it into supplemental motor cortex. That supplementary area. So this is up here again in both cortices, supplemental motor cortex integrates movements. It's involved in bilateral movements, meaning both sides of your body and background movements. So where does my torso need to be if I'm walking? Where does my torso need to be if I'm moving an arm? So background bodily movements in preparation for the primary movement or thing that you're trying to do. That's what a background movement is. Let's see, [paper rustling] I should note too the supplemental motor cortex less understood than the other areas and it works in conjunction with the premotor and the primary motor. But we do understand primary motor cortex. So it is our execution of movement center. Primary motor cortex is what is directing the motor neurons to contract or send a contraction message. So execution of movement is carried out by that primary motor cortex. So fine motor control, your ability to, say, hold a pencil or even your typing on your keyboard. Your very fine motor control in your fingers is due to very direct projections, like not quite one-to-one but very close, down from your primary motor cortex to the motor neurons in your spinal cord. All of these regions do have some mapping. Oh, I forgot to highlight each of the regions. So green was supplemental, and red was your primary motor cortex. Again, that primary motor cortex is right next to that primary somatosensory cortex. I think it really highlights how you need sensory information to move appropriately. So this is your motor homunculus. You remember we talked about that sensory homunculus. And so how your brain sees your body, the sensations of your body. This is how your brain sees movement centers and motor control in your body. You can see that there's, you know, about two thirds of this is devoted to the hand and again to the mouth and lips. So it just highlights where you have a lot of precise one-to-one connections to control motor. So where you need precision, you have a lot more neurons and a lot more directly connected neurons. And if you wanted to compare what they look like between motor and sensory, I just put them together. There's no real point to this other than this is what they look like. And the real point is where you need precision, you have greater representation in your brain. It just reflects where-- how many more neurons you have dedicated to that. Okay, we also have a couple specialized motor regions in our cortex. And so we'll just go through a couple of these interesting ones. We've talked about some of them already. In fact, I think that's the first-- yeah--the first one I want to cover, Broca's area. Nope, I didn't highlight it. So Broca's area here in light blue. Does anybody remember what Broca's area does? Speech production, yeah. So doesn't it make sense that it's in a motor area? So, very much motor control for word formation. Just above that, Sylvian fissure at the base of our premotor area and adjacent to our primary motor cortex. So again, damage to Broca's area doesn't prevent vocalizations, but it prevents coordinations of muscles necessary to form language, whether that is words that are spoken or written. The extent of damage to this region depends on whether you have both hand-based language, whether sign language or writing, as well as spoken language with the mouth is affected. So when you have somebody who has a language impairment, what is that called? Aphasia. Yep. So I want to note real quickly, that is an A term. We are going to have, I think there are five separate A terms relative to neurology. So just preparing you that we are going to have another one of those lists of all these A terms that we have to differentiate. But aphasia is the first one that we have used. So Broca's, damage to Broca's area is a production aphasia. So, as we've talked about previously. All right. Next step is voluntary eye movement fields. So there we go. Oops. Get my pointer. So eye movements here in yellow. You may or may not have experienced this in a neurological exam if you've ever had the doctor come up to you and put a finger in front of you and say, "Hey, follow my finger." So that part of your brain, that part of your cortex, is what does that. And so damage, if you damage that portion of your cortex, you are unable to follow that finger. Or you may inappropriately fix your gaze on something, on some object. Blinking also controlled here, you blink about 15 times a second, which you're now going to count, right? [laughs] Yes. - [Student] The voluntary eye movement, is that also damaged from, oh, I don't know, maybe exposure to ethanol or... - [Professor] It can. It absolutely can. So excess alcohol drinking damages your frontal cortices pretty preferentially. More your prefrontal, but it can absolutely extend back. So yeah. Yeah, so blinking is in your voluntary eye movement field as well. Next up is head rotation. Conveniently located next to eye movement. In fact, you have a lot of coordination between eye movement and head rotation. And that's because when your eyes go somewhere your head needs to go too or vice versa. So it absolutely makes sense that they're close together. So you have a head rotation center and then you have a hand skill center. And so this is specific to things that you do with your hands. Damage to this region is called a motor apraxia. And I'll have this written on another slide. [chalk scratching] So that word isn't on another slide, but just so you see another A starting word relative to neurology, apraxia. A motor apraxia is the inability to execute or carry out a skilled movement. And this is despite having the physical ability or desire to perform it. So meaning your muscles are all in place, your brain wants to make this movement. You are just physically, I guess you should say your brain is unable, you're physically able, but your brain is unable to make that movement. And so it's a motor apraxia. And we'll talk about that again when we get to damage to cortex. Okay. [paper rustling] Okay, so I hinted at this already, voluntary movement information flow. I just want to put this, I just put this in here because this is the big picture of how we react to our environment and do something, have a behavior in response. And so I just wanted you to see how that information flow, I don't, it just helps me for if we sense something and then make a movement in response. And so starting here, sensory cortex, you have detected, whether that is visual or somatosensation or hearing, you know, no matter what the sense is, it goes to its primary sensory cortex. It then goes to some sensory association cortex where it gets integrated with other senses, then we send it to our prefrontal cortex, step three, that's our prefrontal cortex is thinking about it. And then we send it to our premotor and supplemental motor. And that's where we make that motor plan. So we think our brain is like, okay, this is what this looks like for the body. I need to activate these muscles, inhibit these muscles, and it makes that plan, that overall body plan. And then it translates it. When it translates it, it sends that translated information to our primary motor cortex. That primary motor cortex is the execution center is telling the motor neurons of the spinal cord to do it, make that movement or inhibit that movement depending on what you're trying to do. And then in the spinal cord, that's where your lower motor neurons originate and project out to the skeletal muscles that will be contracted. So to spinal cord to contract muscles and make a movement. Again, just how information is flowing. So once we come out of that primary motor cortex, where is information going? So outgoing pathways from the primary motor cortex. So, much of this is going to the spinal cord. So we're going to talk about the corticospinal tract, and then we're going to talk about the indirect path, which is through our red nucleus and reticular formation. So lots of this movement-- direct movement-related information is to the spinal cord. But we also have pathways going to other cortical regions, telling the other parts of our brain, "Hey, I'm making this movement," and to basal ganglia. And we'll get to that on Thursday. Okay, so this--some of these regions that I was just talking about. So to spinal cord direct corticospinal tract shown here in blue. So let's talk about that real fast. So our corticospinal tract, this is very much our execution, especially for fine motor control. These are pyramidal cells. And so we talk about this as the pyramidal tract. This is also our upper motor neurons, and that's because these are the motor neurons going from our primary motor cortex to the spinal cord. And so maybe you already figured that out from cortico--cortex--to spine, so corticospinal. So also called upper motor neurons. These direct connections from our primary motor cortex down to the spinal cord control speed and precision of fine motor. Many of these cross in the medulla, which is what they're try to show here. And so where these fibers cross creates kind of a pyramid. And so they talk about this as the pyramids of the medulla. And also why, you know, part of the reason we talk about this as a pyramidal tract; these are also very large pyramidal neurons as well. So lots of reasons to call this the pyramidal tract. So most fibers cross in the medulla to the other side of the spinal cord. So just like we talked about with sensation, the contralateral. So if you sense on the right side, bulk of it is sent on up to the left side. So for all senses except one, that sensory information crossed. What was the sense that didn't cross? Taste, no idea why, but it doesn't. So same thing for movement. You are controlling the opposite side of your body. So your left hemisphere is controlling your right side of your body; your right hemisphere controlling your left side of your body. So most fibers cross--not all but most-- and then synapse down on inner neurons of the spinal cord. Want to talk really quickly about Betz cells. So these are very unique ginormous pyramidal cells in this corticospinal tract for a cell. So these are like 60 micrometers in diameter, which for me, I study cells that are like 10 micrometers in diameter. So 60 just is--that's huge. Doesn't seem very huge to the naked eye, but at least in the microscope, it's very large. So these giant pyramidal cells are responsible for, you know, these direct connections. So these Betz cells are the fastest efferent route in our brain and body. So they are sending information at about 70 meters per second. This is still half the speed of what we learned about for proprioception. Remember, proprioception is like 110 meters per second. So this is 70, so a little bit slower, but still this is the fastest motor system in our body. So from brain to spinal cord. You have about 24,000 of these. I guess somebody counted them [laughs] so. You know, out of a million, that's a decent amount. And we talk about these. So these Betz cells, again, giant pyramidal cells that are very quickly sending information. Because they're so large, that's one of the reason it helps them send information the fastest. So fine motor control from these very direct projections, from your primary motor cortex down into your spinal cord. Everything when it hits the spinal cord synapses onto inner neurons. There's always inner neurons involved whether or not, you know, our images show that. Okay, you will hear this talked about as the pyramidal tract, especially when you talk about Parkinson's disease next week. You may hear the term extra-pyramidal symptoms. And so when somebody says extra-pyramidal symptoms, they're talking about motor symptoms that are not related to your corticospinal tract. So not related to these pyramidal cells of the motor system. So that is not necessarily the best terminology, but it is still hanging on in our medical circles so. Okay. Oh, again, and yeah, reinforcing, these are upper motor neurons. And then, oh, our lower motor neurons are the motor neurons that start in the spinal cord and head to the muscle themselves. So upper brain spinal cord, lower spinal cord to muscle. All right, flipping back. So our red nucleus pathway, this is an indirect path. And so you can see in red all this information coming into that red nucleus. And so you can eventually get down to those lower motor neurons through this indirect pathway. And that's what I'm going to talk about next. So flipping back up to red nucleus. So this is an alternative tract to the spinal cord. We talk about it as an accessory route. So if you destroy that primary motor cortex, you can still have movement. It may be, not it be as clean, might not be as precise, but you can still have movement and it's through this red nucleus indirect route. You have topographical representation just so your motor cortex I showed you was mapped and you have that same rough topographical map. But again, just not as precise. And if you look at this image, you can see the information going from the motor cortex down to the red nucleus and then down to other motor centers. Our red nucleus is very closely associated with cerebellar function, which we'll talk about on Thursday, which is coordinated, is in charge of timing and coordination of movement. Our red nucleus tends to control distal motor groups and upper limbs. So things that are further out. Less finesse is what happens with red nucleus control. Less precision, less finesse in movement. Okay, I think flipping back, yep, that's all I want to talk about for that, for cortex. Okay, symptoms of cortical damage. And so we group this into, finally pathophys. We group this into positive signs and negative signs. So positive signs are things that are added, they're abnormal. And so that's why when I think positive, I think plus, so I've added something and so positive signs with cortical damage, you get spasticity, which is too much contraction of the muscle. You get exaggerated spinal reflexes, we'll talk about those spinal reflexes on Thursday. So both spasticity and exaggerated spinal reflexes are considered release phenomenon where that damage releases the area from inhibition. So the loss of inhibitory cortical control or cortical input is what drives that spasticity or drives that exaggerated spinal reflex. Again, release phenomenon, it's released from inhibition. So you have, besides like movement being told to go from primary motor cortex down to your muscles, you also have inhibitory information being sent to other muscle groups. And so it's the loss of that inhibitory information that gets turns into spasticity of your muscles or exaggerated reflexes. Another key one is a key symptom of cortical damage is called the Babinski response. So that Babinski response, so this happens in babies. Babies do not have a developed corticospinal tract. It's still forming it, it's still developing, those connections just haven't grown yet. And so when you like rub something across the bottom of the foot, where's my pointer, hello? There it is. When you rub something across the bottom like a pen, yay, somebody's left, rub a pencil across the instep, the arch of a foot on a baby, it causes that toe to stick up. So just like this. Now if you do this in an adult, if that toe sticks up, it is a sign of cortical damage. And so you can Google this if you need to see like an image, I'm sure there's a YouTube video that shows this, but at that Babinski sign, so when that toe sticks up, when somebody rubs like a pen or pointer across the foot, that Babinski sign means there's cortical damage so. All right, so I'm going to go ahead and stop here. And that will let us pick up with the negative signs on Thursday. I will be in office hours today if anybody needs anything, and see you guys on Thursday. [inaudible background conversations] - [Student] Okay, so verification of what we discussed today. - [Professor] Uh-huh. - [Student] So instead like-- - [Professor] Yes. - [Student] [inaudible] - [Professor] It's just to show you the difference between like standard innervation versus a direct. - [Student] So this isn't direct here? Just so-- - [Professor] No, no, they're just trying to show you--[faintly speaking] Yeah, yeah, just trying to show you how the adrenal medulla looks different but yeah. - [Student] Are all autonomic reflexes like regulated by the [inaudible], or have like just-- - [Professor] You've got--you do. - [Student] Okay. - [Professor] You have had-- there's urination. t's the ones that are down in the lower half of your body are spinal cord. - [Student] Those are limbic- - [Professor] But so like the upper ones, those kind of go through the- - [Student] The upper ones going the medulla. Yeah, and this is parasympathetic. So cranial, sacral, your sacral functions on those autonomic control centers are sacral. - [Student] Okay. Thank you. - [Professor] I probably will never ask anything that detailed. - [Professor] Okay. [Professor laughs] - [Student] So yeah. - [Student] I was going to ask real quick. For the exam for like the fill-in-the-blanks, do you get partial credit if you get parts of it right? - [Professor] Oh, it depends. - [Student] Okay. - [Professor] And I--so spelling, as long as it doesn't change the meaning of the word, I accept just about everything. - [Student] Okay. - [Professor] I see everything. And so whether you wrote, I can't talk too much, whether you wrote a letter or the word or whatever, however close you get, so there's lots of partial. - [Student] Okay, but if it was like two different parts to it and you got one part right and one part wrong, do you get like partial- - [Professor] You get partial. - [Student] Oh, awesome. - [Professor] Yeah. - [Student] All right, thank you. - [Professor] And I haven't graded any of that. I won't grade it till probably Thursday. - [Student] Oh, all right. - [Professor] Because the last test is Friday. - [Student] Oh, awesome, all right. [inaudible background conversations] [paper rustling] [inaudible background conversations] [inaudible background conversations] [inaudible background conversations] [student laughs] [inaudible background conversations] [inaudible background conversations] [inaudible background conversations] 2. 10/17/2024(Thur) - [Professor] All right, good morning. [inaudible background conversations] So last day of physiology. We finally will get to move in. I have a little bit of patho mixed in. Obviously, we stopped with a little bit of patho. But yeah, next week and the week after is all patho. So all much more interesting and much more fun. What we've been waiting for all semester. - [Student] We can't hear you. - [Professor] With that questions from last time, talking about cortex. - [Student] Dr. Nixon? - [Professor] Yes. - [Student] I apologize to interrupt. I think your microphone is not working. - [Professor] Thank you. - [Student] Thank you. - [Professor] Oh, it's because it's down there. [students laughing] - [Professor] Okay. Better? - [Student] Yes. - [Professor] Yeah, when it's on the floor by your feet, it does not pick up voice. So, anyway, sorry about that. Yeah, first of many technology problems. I feel very lucky that my computer's even working this morning because neither my desktop nor my laptop would work for a period of like 15 minutes. I'm sure it was some pushed update. So, anyway. So, any questions about cortex and its role in voluntary movement? That's a hair going up, not a question. [laughs] Okay, well, good deal. And some of this will definitely get reviewed as we talk about the patho piece of things. Okay, so we left off talking about symptoms of cortical damage and positive signs, meaning things that are added, abnormal behaviors. So we talked about spasticity, which comes about from too much contraction. And that is because your cortex is sending a lot of negative signals or inhibitory signals. And so this is a release phenomenon, and it's releasing those muscles and causing too much contraction. You also get exaggerated spinal reflexes. This will make a little bit more sense when we actually talk about those spinal reflexes towards the middle of class today. And the Babinski response. So where you take a pointer, pen, or something, and run it across the bottom of the foot. And if in an adult that toe sticks up, called the Babinski sign, that means there's damage to your cortex. That Babinski response normally happens in babies, and that's because their corticospinal tract is not yet developed. So you would expect that. Okay, so negative signs. So things that we lose, behaviors that are lost. The first one is hypotonia. So loss of tone in your muscle. I want to note that we see hypotonia no matter-- you know, regardless of region that's damaged. We'll see this in a number of different places. And so this isn't necessarily pointing out cortex per se. So hypotonia is loss of muscle tone or decreased muscle tone. It's really more like less resistance to movement in the muscle. Not the same as muscle weakness. So, definitely, want to point that out. I'm going to trip on this. But you can have both hypotonia and muscle weakness occur at the same time. So that can get a little tricky, but that's why we have physical therapists and doctors that can kind of tease that apart. The next one up is, of course, loss of sensation. So if you damaged sensory cortex, especially, your somatosensory cortex, this absolutely impacts movement and motor control. You have to have sensation. You have to have proprioceptive information about the state of your muscle and the length of the muscle or joint angles, knowing where your muscle is in space in order to have correct motor control. And we'll talk a little bit about that as we talk about muscle stretch receptors here in a few minutes too. So loss of sensory cortices, damage to sensory cortex, absolutely, impacts motor control. Apraxia. So we talked about apraxia when we talked about hand skills. So apraxia, another one of those a starting neurology terms, is your inability to carry out a skilled movement. And again, we talked about it relative to hand movements. And again, these are things that are a skill. So your ability to write is a skill. Your ability to type is a skill. Play piano or an instrument, all those things are skills. And so inability to carry out that skilled movement, something you've had to learn or practice. And again, not due to muscle weakness or some sort of sensory loss, very specifically, a motor piece of this. And then, finally, a negative sign of cortical damage, aphasia. So Broca's aphasia. So your inability to produce words. So, hypotonia, damage to cortex, sensory cortex, apraxia and aphasia, all the negative signs of cortical damage. All right, are we ready to move on to- Or I should say, any questions on cortex? Okay, so next up we're going to talk about basal ganglia. And so as I warn, this is a little bit complex, but I'm going to try and simplify it as much as possible. And we'll talk about this twice. We're going to talk about it here today and really introduce some of these concepts. And then we'll reinforce this when we talk about Parkinson's disease and start to hint at and build a case for the dopaminergic treatment in Parkinson's disease or manipulating the dopamine system from multiple ways. Oh, I put this in here just to remind you that basal ganglia kind of fits up under here. So if your cortex is here, that basal ganglia is kind of down the base, hard to see from this side view, sagittal view, but hopefully we will try to look at it a little better in the next slide. Also, five nuclei of the basal ganglia. I don't necessarily require you to memorize these, but you do have to recognize them. You do have to, you know, if you see a sentence that uses these terms, you need to be able to go, oh, that is basal ganglia. She's talking about basal ganglia. And especially, as we talk about disorders of basal ganglia next week. So five nuclei that we'll talk about, the caudate, the putamen, collectively, we call these the striatum, the globus pallidus, so our primary output, and our input in the striatum and then output through the pallidus, substantia nigra, and subthalamic nucleus. So those are the five nuclei. And again, I put these in, these are terms that get used in talking about Parkinson's disease, and so we've got to understand what they mean. Okay, so here is dreaded slide of basal ganglia. Keep this simple. Keep this take-home message in mind. Because we're going to have a little bit of anatomy, a little bit of physiology, a little bit of pharmacology. And all of this is so that we can understand the pathophys and even start to touch on potential pharmacotherapy approaches. So take-home message is this direct pathway in green, is what enables movement, while this indirect pathway in red is what inhibits movement. All right, so starting on the left. And so this is that coronal section. So here's all that cortex on top, and here is the basal ganglia. As I said, it's tucked deeply underneath that cortex. So we're looking at a couple different things here. Get my pointer going. So some of the key things, and I try to do this better every year. So I'm hoping this approach this year is the way to talk about this. I think one of the key things I want to start with is, so motor output, primary motor cortex here, two spinal cord. So this is in green. Green in this left side is glutamatergic. So think about this as our primary excitatory neurotransmitter. This is a fast EPSP-driven "move that muscle" signal. And so that always comes from our primary motor cortex down to the spinal cord. So we are going to be talking about basal ganglia role in movement. Well, that basal ganglia role is due to its influence on motor cortex activities. And so you'll see signals going from the basal ganglia to that motor cortex to tell that motor cortex what to do. So I'm trying to back us up into the basal ganglia. Okay, so hopefully, that helps. So we're going to talk about how that basal ganglia functions. We're going to talk about this direct versus indirect path and how that has a net effect on that output to motor cortex which directs the movement through its projections down to spinal cord and motor neurons. Okay, so once again, green is a glutamatergic signal. Red is an inhibitory signal, and this is GABAergic. And so where you see these red arrows. And then, finally, dopamine is in blue, and you can see it's just this little dashed line that's in blue down here. So, again, there's a method to my madness here. We're introducing this pharmacology, because we're going to be talking about this when we get to Parkinson's disease. Parkinson's disease is a loss of these dopaminergic cells. And so that's why there's such an emphasis on that. And you don't have to write that down right now. I see you guys all writing that. We will talk extensively about that. Just want you to understand where we're going. So we're going to talk about how these two different paths affect that motor output. - [Student] So why is the blue important? Again, like, I understand the direct and the indirect, but the blue doesn't have the keys, so. - [Professor] Well, we'll get there. Yep, we'll get there. So just bear with me for a minute. Also, in here and there, we don't have a color for it, and we're not talking about, there are a bunch of cholinergic inner neurons within that striatum itself that we will definitely talk about when we get down to Parkinson's disease. Okay, so remembering motor cortex is that primary output, how does that influence that primary output? So striatum itself. So that is the caudate and the putamen. So right here, that is our input pathway into basal ganglia. And you can see there's motor information coming into that basal ganglia. So principal input structure is that striatum. This is all excitatory glutamate information. It's coming from multiple areas of the cortex, not just motor cortex. So some sensory cortex, all sorts of information telling your brain, "Okay, I'm going to be moving, and I need to coordinate these activities." So all of that coming in. Once it comes in, you have these two separate tracks, you have this direct pathway, again, enabling movement, and you have this indirect pathway that's inabling, so inhibits movement. So once it comes in, we can trace that direct path. And you know it's got D1. So that D1 is that direct path has a bunch of D1 type of dopamine receptors. And so you can come in, hit that direct pathway. And that direct pathway here, so it comes into the putamen, goes through the other nuclei of the basal ganglia and then heads straight out to the thalamus and then back to the motor cortex. So direct, it's a direct path in and around the basal ganglia and then out to that motor cortex to enable movement. Makes sense to me. This is the tract, the direct path is directly telling the motor cortex to move. Now, the indirect path is very indirect and this is where all those arrows come in. And so we still come into the striatum, but then we go around to all these different nuclei and then back again to that globus pallidus, which finally lets us go back out to the thalamus and to the motor cortex. So indirect is indirect and it goes through all the different nuclei and eventually passes to the motor cortex. That indirect pathway has D2 receptors, so Gi inhibitory D2 receptors. And this is the inhibitory. So it inhibits movement. And so I can remember this because D2 are Gi inhibitory, and this is the inhibition, indirect. So all those I's, so inhibiting our movement. All right, so take home message from this is that dopamine action within this signaling pathway is helping to enable movement. But dopamine action through these D2 inhibitory signals also inhibits movement. So we can leave it right there for how this functions under normal conditions. Some of you're like, ah, Dr. Nixon. So little foreshadowing ahead. So if Parkinson's disease is characterized by the loss of those dopaminergic inputs, which we'll talk about, that means you are losing your inhibition. And so you're having too much movements in the case of Parkinson's disease, too much contraction. But for those of you that have ever studied Parkinson's disease, you're like, Dr. Nixon, that makes no sense. They have trouble moving. Too much contraction of the muscle, stiffness, spasticity can all contribute to that inability to move. But we'll get there. So today's little piece of this and we'll build onto this next Tuesday, is that we have this direct pathway that enables movement through our D1 receptors, and we have this indirect pathway that inhibits movement through our inhibitory D2. All of this coming into the striatum, all of this eventually feeding out to the motor cortex to direct that movement. So it's influencing. This structure, basal ganglia, in general, is very inhibitory, so it kind of inhibits movements that you don't need while you're trying to make a primary movement, all of that feeding through that motor cortex. Questions on that? Don't go too far because we will for sure come back to this. Yes. - [Student] I'm not going to go too far. So you have like, you set for the direct pathway, it's from the motor cortex to the spinal motor neurons, right? - [Professor] And so all of this feeds back to that motor cortex, and it's because your primary motor cortex is what's executing movement down through the spinal cord, through its projections to the spinal cord. - [Student] So it starts in the motor cortex, goes to the spinal cord and back to the cortex? - [Professor] Yes. So movement in general is being executed by that motor cortex. Basal ganglia is influencing that motor cortex. And so the direct versus indirect pathways influence that motor cortex output. All right. We get to hold there for a couple days. Okay, so that's basal ganglia. We'll find out if I did that right or did that better. Every year--I've been teaching on this I don't know how many years, and everybody's always like, oh my goodness. [laughs] So, all right, cerebellum, - [Student] Wait. Sorry, one more question. - [Professor] Yeah. - [Student] The caudate is the input, and the putamen in is the output? - [Professor] The caudate and putamen, that is your striatum, and that's input. So in together, it's input. But you can trace--you can kind of see. It goes to the putamen first. Okay. All right. Cerebellum. Cerebellum, much easier. So we already talked about cerebellum and its general role. So it is timing and coordination of movement. And we know this very strangely. So if you electrically stimulate the cerebellum, there is little to no sensation, and there is no motor response. So people, I'm sure when they first did this, were like, "Well, what does this do if we can't-- you know, if you stimulate it, it doesn't do anything." But if you remove it, then the result is total incoordination. You are completely uncoordinated. Think about--the word that we're going to use is ataxia. So another A word. And I have that spelled down the road in another slide. So ataxia is essentially uncoordinated movement. Think about somebody who is exceptionally intoxicated trying to walk down the street. Like how many times have you walked down Sixth Street yourself, and you're like, "Oh, they're not in a good place"? My poor rats right now. [laughs] Yeah, we have a bunch of rats who are drunk. And they are ataxic; they are stumbling just like humans. That's why we use them as a model. So they cannot walk. They're not coordinated. They're stumbling. And some cases, their little feet can't even get up underneath them. So just a hot mess [laughs]. Incoordination. And so that is very much cerebellar. In fact, your cerebellum is packed full of NMDA receptors. And wouldn't you know it, alcohol inhibits those NMDA receptors. And so all of that ataxia is very much due-- in the case of alcohol intoxication-- is all due to that alcohol inhibiting those NMDA receptors. The point I want you guys to remember is that cerebellum is coordination. And so if you inhibit that cerebellum in some way, you're going to have total incoordination or lack of coordination. So what goes into that is the timing and the intensity of your muscle contractions. And so that cerebellum is just a few milliseconds ahead of what you're actually about to do. And so it can control the timing of contraction of particular muscles or the intensity or how many of those muscle fibers get contracted. And that helps to ensure smooth action within a larger muscle group. It also sequences motor activities. So it's constantly monitoring and making adjustments when movement is occurring. And this especially occurs between our antagonistic muscle pairs. So we'll talk a little bit about this today. When we say antagonistic muscle pairs, it's just that for all your major limbs, you have a flexor, say, in my bicep, as opposed to an extensor, my tricep. And so your cerebellum is coordinating the contraction of one of those but inhibition of the other. And so if that gets screwed up, again, you're a total mess, completely uncoordinated. So very, very important. The great thing about your cerebellum is it learns from itself. So if the movement is not consistent with what you intend to do, it will change that coordination, it'll change the timing, it'll change the intensity of that contraction, and it will essentially change the strength or the weakness of what it's directing those muscles to do. And so practice makes perfect in the cerebellum. And again, it is evaluating what you intend to do versus what you actually do. And so we call that the comparative function, or the comparator function, of our cerebellum. So comparing intent. And so this is your brain sending that signal down; you get a little offshoot to the cerebellum saying, "Hey, this is what I'm about to do in the body." And then versus what actually happens. And that, actually, is all that proprioceptive information coming back up to the cerebellum and going, "Oh, well this is what actually happened." So if that intent does not match with the proprioceptive information of what actually happens, the cerebellum tweaks the system. Oh, this one picture before I leave this is- I'm about to talk about the comparative function just a smidge more. So there are a couple different lobes. I should say there's a couple different lobes, but there's also these functional regions and it's always very funny that the lobes don't correspond to the functional regions. And that's why you just have these kind of stretching across the cerebellum. So we have the spinocerebellum, and this is where that comparative function is. So it's comparing the proprioceptive information about what actually happened with your motor plan coming d

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