PSYC 275 Exam 2 Notes PDF

Lecture 8 Neuronal Signaling pt. 1 (electrical communication) RESTING MEMBRANE POTENTIAL ○ Membrane potential → difference in the electrical charge between the inside and outside of a cell. The electrical difference across the membrane at rest...

Lecture 8 Neuronal Signaling pt. 1 (electrical communication) RESTING MEMBRANE POTENTIAL ○ Membrane potential → difference in the electrical charge between the inside and outside of a cell. The electrical difference across the membrane at rest It is -70 mV. The inside of the neuron is more negative compared to the outside (more negative by -70 mV) At rest, a neuron is POLARIZED (pos charge outside, neg charge inside) Sodium Ions and potassium Ions maintain the resting potential of a neuron At rest → more sodium outside than inside At rest → ion channels that allow sodium ions to move across membrane are CLOSED Sodium ions are positively charged Sodium ions are under constant pressure to enter the neuron 2 forces acting on the sodium ions: electrostatic force (positive and negative attraction) and the concentration gradient of sodium ions ○ Ions tend to move from areas of higher concentration to areas of lower concentration At rest → more potassium ions on inside than on outside At rest → potassium ion channels are closed ○ Ions are under electrostatic pressure to stay inside the neuron ○ Potassium ions are positively charged ○ Inside of neuron is negatively charged Some of the ions will leak inside and outside, which are counteracted by the sodium-potassium pump ○ For every 3 sodium ions moved outside by the pump, 2 potassium ions are moved inside by the pump ○ They are actively transported back if they leak by the pump to where they should be POLYSYNAPTIC POTENTIALS ○ Presynaptic to Postsynaptic communication  One cell activates another cell; the space between cell body and synaptic button is the synapse. In here, chemical communication between two cells takes place Presynaptic neuron (before the space) communicates to the postsynaptic neuron using neurotransmitters (chemical messengers) Neurotransmitters bind to postsynaptic receptors and cause the resting membrane potential of a neuron to change. It can either become less negative or more positive (depolarization). This change is an excitatory post-synaptic potential The opposite? Inhibitory post-synaptic potential. Neurotransmitters activate the receptors and cause the potential to become more negative or less positive (hyperpolarization) ○ Postsynaptic potentials are graded This means the size of the postsynaptic potential (excitatory or inhibitory) depends on the strength of the signal that is activating the potential ○ Two characteristics of postsynaptic potentials Travel very fast As they travel from area of origin and move outwards in the cell membrane, their size decreases. They are “decremental”. Eventually they completely fade as they travel long distances ○ A single postsynaptic neuron receives ten thousands of signals from presynaptic neurons; they are a mix of excitatory and inhibitory. Responses are all combined to produce a net-effect at the axon initial segment Either a net excitation or net inhibition or no response at all Purpose of integrating all these potentials? To decide whether to activate an action potential or not in the axon that will then travel down the axon and activate the end of the neuron To activate the potential, the neuron needs to be depolarized (-70 mV to -65 mV). This is the threshold. If the net effect results in membrane potential being more negative than -65 mV, then there will be NO action potential If the net effect is less negative than -65 mV, an action potential is generated Two types of integration of postsynaptic potentials  Integration taking place over space (spatial summation) ○ EPSPs and IPSPs are generated at the same time but in different locations ○ Two EPSPs or IPSPs sum to produce a greater postsynaptic potential Integration taking place over time (temporal summation) ○ EPSPs and IPSPs are generated at different times but in the same location ○ Two EPSPs or IPSPs are elicited in rapid succession sum to produce a larger postsynaptic potential ACTION POTENTIAL ○ Very short lasting change in the membrane potential, where the potential goes from a large negative number to a large positive potential (-70 mV to +65 mV) and then back again to -70 mV ○ Can travel in 1 direction along the axon because of the absolute refractory period ○ How do action potentials provide indication of strength of signal? Not by amplitude, but by FREQUENCY of stimulation. Max frequency is 1000 hertz ○ Slower compared to postsynaptic potentials, but are non decremental. They dont decrease in size as they travel away from site of origin ○ Antidromic conduction → if it is travelling in the opposite direction it normally would ○ Orthodromic conduction → if it is travelling in the same direction it normally would ○ Effects of myelination on conduction? In betweens exposed regions of axons (“NODES OF RANVIER”), there are sodium and potassium channels where an action potential can be generated. The rest of the segments are insulated so an action potential is NOT generated in the insulated area. “Saltatory conduction” allows instantaneous conduction of an action potential from one node of ranvier to another Myelination makes a potential much faster, allowing the potential to jump over large differences ○ Diameter of the axon on speed of conduction? The larger the diameter, the higher the speed of conduction ○ Interneurons  Special case: either no axons or small axons Conduction takes place mostly through postsynaptic potentials rather than action potentials ○ Differences between action potential vs postsynaptic potential? The size of an action potential is not graded. It is not dependent on the strength of the incoming signal. Its an ALL OR NONE response and its size will be the same regardless of the incoming signal that initiated it ○ Net postsynaptic potential at axon initial segment Threshold → if the membrane potential is more than the threshold, an action potential will be generated -65 mV → depolarization → Sodium channels open → sodium ions rush inside the cell and make the inside of neuron less negative → -45 mV → potassium channels open → potassium ions leave the neuron → +50 mV → sodium channels close so the inside of the neuron stops becoming positive → the neuron becomes less positive → -70 mV is reached → potassium channels close while the membrane potential is hyperpolarized, more negative than -70 mV → more sodium inside and more potassium outside → sodium-potassium pump and random movement of ions kick in → the charge of the inside of the neuron is then restabilized thanks to the pump and leaking of ions Refractory period Absolute refractory period → a duration in which no amount of stimulation to the neuron can stimulate another action potential. The sodium channels are now closed and can’t be caused to be open during this period, leaving the action potential with only one direction to travel Relative refractory period → a duration at which an action potential can be generated, but the amount of stimulation required is much greater than normally required Lecture 9 Neuronal signaling pt. 2 (chemical communication) SYNAPTIC STRUCTURE ○ Axodentritic synapse Synapse is area between two cells where chemical communication takes place Ends of an axon (synaptic button) contact the dendrites of a neuron The postsynaptic site of contact has a swelling called the “dendritic spine” ○ Other synapse types Axon contacts the soma (cell body) of a neuron → axosomatic synapse Axon contacts another axon → axoaxonic synapse Myelin contacts the axon → axomyelenic synaps Synaptic contact between dendrites → dendrodendritic synapse ○ Synapses can be broadly categorized into two types Directed synapses → the presynaptic and postsynaptic neurons are in close proximity to each other. The site of release and reception of NTs are close together Non-directed synapses → the pre and postsynaptic neurons are far away, and the presynaptic release of NTs take place at swellings (“varicosities”) along the axon. Once NTs are released from these swellings, they have to travel a long way. Varicosities give axons the appearance of beads on a string NT SYNTHESIS ○ Two broad categories of NTs: Small NTs Made in the cytoplasm of the synaptic terminals instead of the cell body In the cytoplasm, there are the golgi complexes that are in the terminals. They package NTs in these vesicles. The vesicles are located close to the presynaptic membrane Activate ionotropic receptors Large NTs Small chains of amino acids Known as “neuropeptides”  Arrange from 3-36 amino acids Made in the cytoplasm of the cell body using ribosomes Placed inside spherical vesicles by the Golgi complexes that are located in the cell body These vesicles are then transported from the cell body down the axon and to the synaptic terminal through “microtubules” ○ Microtubules → railroad tracks that move vesicles from one cell region to another, to the synaptic terminal Vesicles are located close to the presynaptic membrane Activate metabotropic receptors A single neuron usually contains a neuropeptide AND a small NT = “coexistence” Coexistence of 2 small NTs has also been noted NT RELEASE ○ Exocytosis → Synaptic vesicles are close tot he presynaptic neuron. The contents of the vesicles are released The cell membrane of the presynaptic vesicles fuse with the postsynaptic membrane. Once theyre fused, the contents are released into the synapse The NTs then activate postsynaptic receptors The trigger for the release of NTs and exocytosis is an influx of calcium ions in the presynaptic membrane. The calcium enters the presynaptic neuron only when an action potential arrives at the synaptic terminal Release of small NTs and neuropeptides vary Small → since they are close to the presynaptic membrane when an action potential arrives and causes calcium to enter the presynaptic neuron, the arrival of the action potential triggers the release of small NTs in pulses ○ Small NTs are aggregated near the membrane where there are a lot of voltage-gated calcium channels. It is a rapid pulsing release Neuropeptides → a slow, gradual process because the synaptic vesicles are farther away from the calcium channels  ○ There needs to be a gradual increase of firing rate of action potentials which causes a gradual increase in the release of calcium NT ACTIVATION ○ NTs have to bind to postsynaptic receptors and activate the postsynaptic neuron ○ Postsynaptic receptors: Essentially, proteins containing the binding site for a few NTs Anything that binds to a protein is a “ligand” of that protein NTs are the ligands of receptors Ionotropic receptors → Ion channels When NT binds to receptor, it leads to an opening or closing of these channels Quick to activate Effects are short-lasting, less diffused, and less variable Metabotropic receptors → more common than ionotropic receptors Structure and sequence → the receptor is a small pink part that the NT binds to. Its located outside the cell. The receptor is attached to a long signaling molecule that winds 7 times across the cell membrane. On the inside surface of the cell, there's another protein (“G protein”). The binding activates the G protein. Then, the G protein causes a subunit of the G protein to dissociate and travel across the membrane. The, it can either bind to ion channels and open or close them OR it can activate other downstream signaling pathways. Slower to activate Effects of activating these receptors last a longer time, are more diffused, and are more variable Autoreceptors → special category of metabotropic receptor ○ Located on the presynaptic neuron ○ Autoreceptors bind to its OWN NT. function is to regulate the amount of NT being released from the presynaptic neuron. If there is too much, receptors will be activated more, causing a reduction in release. If there is too little,  the receptors will be activated less, causing decreased release of NT ○ Involved in the feedback regulation in the amount of NTs released from the synapse Lecture 10 Neuronal signaling pt. 3 (chemical communication pt. 2) NT DEACTIVATION ○ NT needs to be deactivated after activating a neuron ○ 1. NT can be taken back up into the presynaptic neuron through transporter proteins ○ 2. NT can be broken down by enzymes (degradation) and the pieces are taken back up into the presynaptic neuron ○ Both systems are very efficient; the NS doesnt waste NTs ○ The synaptic vesicles that were fused with the presynaptic neuron are then drawn back into the presynaptic neurons to create new vessicles GAP JUNCTION ○ Electrical communication taking place between neurons ○ Takes place through channel proteins known as “connexins” Tubular proteins that allow direct contact between pre and postsynaptic neurons They allow electrical signals AND small molecules to pass through The speed of transmission through electrical signals is FASTER than chemical communication ○ Some functions for gap junctions: To link astrocytes in a network, allowing for connectivity and continuity Link inhibitory interneurons of the same type and activity NT CLASSES AND FUNCTION ○ 4 subcategories of small NTs: Amino Acids Glutamate → common in the proteins we consume, most common excitatory neurotransmitter in the NS. neurons that release glutamate are known as “glutamatergic” Aspartate → common in the proteins we consume. Neurons that release this are “aspartergic” Glycine → common in the proteins we consume. Neurons that release this are “glycinergic” GABA → most common inhibitory neurotransmitter in the body, BUT has excitatory effects in some synapses. NOT an excitatory  acid by itself, but is synthesized by glutamate. Glutamate is converted into GABA by modifying its structure Monoamines Catecholamines → made from Tyrosine, which is converted into L-dopa, converted into dopamine, converted into epinephrine, converted into norepinephrine Indolamines → made only from Serotonin, which is converted from tryptophan Acetylcholine Only acetylcholine, a category of its own NT that is released from neurons onto the skeletal muscles, causing them to contract Also found in the CNS and in the autonomic nervous system Unconventional NTs Soluble gases → nitric oxide and carbon monoxide Endocannabinoids → anandamide Unconventional because they affect te PREsynaptic neuron rather than the postsynaptic neuron Role in retrograde transmission. Transmit signals from post to presynaptic neuron, regulating activity of the presynaptic neuron ○ 5 subcategories of neuropeptides: Named based on the area of the body they are found in Pituitary peptides Hypothalamic peptides Brain-gut peptides Opioid peptides Miscellaneous peptides (if they fall into none of the other 4) Lecture 11 Research Methods TECHNIQUES TO VISUALIZE THE BRAIN ○ Computed tomography Looks at structural anatomy of the brain Provides researchers the ability to visualize internal structures of the brain During a CT scan, participant is placed inside scanner. Inside the scanner, a source of x-rays emits x-rays. On the opposite end of the scanner, theres an x-ray detector. The patient is in between the source and detector. Whatever scans are not absorbed by the brain tissue are absorbed at the x ray detector Diff components of the brain will absorb x rays to a diff extent The whole setup then rotates and the scan is taken from a diff angle. The process is repeated several times Once all the xrays are taken, all sections are combined to make a 3D representation of the brain ○ Positron Emission Tomography Visualizes the activity within diff regions of the brain; a functional brain image The participant is injected with a radioactive substance in their carotid artery (may be FDG, fluorodeoxyglucose) One of the hydroxyl groups bonded to glucose is replaced with an oxygen, and fluorine is radioactive FDG cannot be metabolized, but the brain and neurons think its glucose so they will take it in The higher the activity in a brain region, the more glucose (or FDG) it will take in. Higher FDG accumulation = higher radioactive signal Participant is placed inside the scanner, and higher radioactivity is detected by the PET scanner ○ Magnetic Resonance Imagine Provides a structural image of the brain Diff between MRI and CT? Structural images provided by an MRI are of a higher spatial resolution, and MRI can produce 3D images of the brain  Participant gets inside the MRI scanner, and around them a very strong magnetic field is applied MRI scanner then captures these scans of signals that are emitted by the participant's body and brain. Based on these signals, a structural image is made What are the signals? ○ The majority of the brain is composed of water. Each hydrogen atom has a polarity. Without a magnetic field, the diff hydrogen atoms of a water molecule are oriented randomly. ○ As soon as a strong magnetic field is applied, all protons align themselves instantly in the direction of that magnetic field ○ As soon as the protons align themselves, they emit a signal. That signal is then measured by the MRI ○ Diff areas of the brain have diff amounts of water in them. Because of this, the strength of this signal will also vary depending on the amount of water in diff areas of the brain TECHNIQUES TO STIMULATE THE BRAIN PSYCHOPHYSIOLOGICAL RECORDING LESION TECHNIQUES ELECTROPHYSIOLOGICAL RECORDINGS