Neuron PDF

The Neuron Best estimate is that brain has 85 billion neurons Neuron is the primary functional unit of the nervous system Neuron is a nerve cell Structures extending from left side of neuron (tree branch) called dendrites ○ Dendrites are where neurons receive most of t...

The Neuron Best estimate is that brain has 85 billion neurons Neuron is the primary functional unit of the nervous system Neuron is a nerve cell Structures extending from left side of neuron (tree branch) called dendrites ○ Dendrites are where neurons receive most of their information ○ Dendrites have receptors that are designed to pick up signals from other neurons which come in the form of chemicals called neurotransmitters The soma or cell body interprets the signals picked up by dendrites (that cause electrical changes in a neuron) ○ Soma contains the nucleus --> contains DNA/genetic material of the cell ○ Soma takes the information from the dendrites and puts it together in area called the axon hillock If the signal from the dendrites is strong enough, it is sent to the next part of neuron called axon ○ This point the signal is called an action potential Action potential travels down axon --> its covered in myelin (insulator material that helps prevent signal from degrading) ○ Last step is axon terminals aka synaptic buttons When signal reaches axon terminals, it can cause release of neurotransmitter  ○ When neurotransmitter is released from axon terminals it interacts with receptors on the dendrites of the next neuron, and repeats process with next neuron Neuron Synapse - Synaptic Transmission Most communication between neurons occurs at a specialized structure called a synapse ○ Synapse is area where 2 neurons come close enough that they're able to pass chemical signals from one cell to another The neurons aren't actually connected, they're separated by microscopically small space called synaptic cleft ○ 40nm wide Neuron where the signal is initiated is called the presynaptic neuron ○ In it there are chemical signals called neurotransmitters that are packaged into small sacs called vesicles ○ Each vesicle can contain thousands of neurotransmitter molecules Neuron that receives the signal is the postsynaptic neuron When presynaptic neuron is excited by electric signal of action potential, the vesicles fuse with the presynaptic membrane and release their contents into synaptic cleft ○ Once they're in, neurotransmitters interact with receptors on the postsynaptic membrane ○ They bind to the receptors and can cause an action to occur in the postsynaptic cell as result Eventually the neurotransmitter molecules must be cleared from the synaptic cleft ○ Some drift away in process called diffusion  ○ Sometimes the neurotransmitter is taken back up into presynaptic neuron in process called reuptake Once back inside the presynaptic neuron, the neurotransmitter can be recycles and reused ○ Other cases, enzymes break down neurotransmitter within synaptic cleft Then component parts of neurotransmitter can be sent back to presynaptic neuron to make more neurotransmitter Neuron Action Potential Action potential is a momentary reversal of membrane potential that is the basis for electrical signaling within neurons Resting membrane potential of neuron is around -70 millivolts When neurotransmitters bind to receptors on the dendrites of a neuron, they can have a depolarization effect on neuron ○ This means they make the membrane potential less polarized, or causing it to move closer to 0 When neurotransmitters interacting with receptors causes repeated depolarization of the neuron, eventually the neuron reaches its threshold membrane potential ○ In neuron with membrane potential of -70 mV, threshold is generally around -55mV When threshold is reached, sodium channels open, allowing positively charged sodium ions into the cell ○ This causes massive depolarization of the neuron as the membrane potential reaches 0 and then becomes positive  Known as rising phase of the action potential The influx of positive ions creates the action potential which then travels down the neuron Eventually action potential reaches its peak --> sodium channels close and potassium channels open which allows potassium to flow out of cell ○ The loss of positive potassium ions promotes repolarization aka falling phase of action potential The neuron returns to resting membrane potential but overshoots it and the cell becomes hyperpolarized ○ During his phase called the refractory period, its difficult to cause the neuron to fire again Eventually the potassium channels close and the membrane returns to resting membrane potential ready to be activated again The signal generated by the action potential travels down the neuron and can cause the release of neurotransmitter at the axon terminals to pass the signal to the next neuron Neuron Spatial & Temporal Summation Action potential goes down the axon of Neuron 2 making an excitatory post synaptic potential in the target cell ○ The depolarization spreads passively within target cell until it reaches the axon hillock ○ Since the depolarization is lower than the excitation threshold there is no action potential generated - resting potential is resumed Activating Neuron 2 in short intervals brings to summation of the excitation in the target cell --> temporal summation If the depolarization at the axon hillock exceeds the excitation threshold, an action potential is generated Action potentials arrive from Neurons 1 and 2 at long intervals ○ The excitation induced by Neuron 1 diminishes before the excitation induced by Neuron 2 arrives --> no action potential is generated  When both neurons simultaneously excite the target cell the excitation builds up --> spatial summation ○ If the depolarization at the axon hillock exceeds the excitation threshold, action potential is generated An action potential goes down the axon of Neuron 3 ○ Leads to an inhibitory post synaptic potential in the target cell ○ The negative charge (blue dots) spreads within the target cell causing cell to hyperpolarize The membrane potential declines further from the excitation threshold Action potentials simultaneously arrive from excitatory Neuron 1 and inhibitory Neuron 3 ○ Excitatory potential merges with inhibitory potential so the membrane potential remains unchanged (red and blue are blending) An action potential arrives from Neuron 3 and causes target cell to hyperpolarize ○ When the membrane potential begins to return to its resting potential, excitation is simultaneously triggered by neurons 1 and 2 ○ The temporal and spatial summation of these potentials initiate an action potential at the axon hillock of the target cell Spatial Summation --> various dendrites receive same input at the same time Temporal summation --> same dendrites receive the same input repeatedly over time ○ Same input = all excitatory or all inhibitory Neuroscience - 6 key neurotransmitters + agonist and antagonist mechanisms Neurotransmitters -> the neuro chemical that communicate between neuron ○ In the synaptic gap neurotransmitters flow from 1 axon terminal, to synapse, and attach to dendrite of another neuron in post-synaptic receptor sites Neurotransmitters are fundamental to thoughts, feelings, learning pleasure Neurotransmitter types 1. Glutamate ○ Major excitatory neurotransmitter in the brain ○ Widespread, very common ○ Especially associated with learning and memory ○ Excitation -> a neurotransmitter is released, attaches itself to dendrite of next neuron, and increases electrical activity in cell body of that neuron - excitatory ○ Too much excitation in certain parts of brain leads to seizures ○ Schizophrenia Glutamate hypothesis: people with schizo have deficiency in sensisity/function of Glutamate receptors 2. GABA ○ Major inhibitory neurotransmitter widely spread throughout brain ○ Associate with distorted levels of anxiety, motor control ○ GABA causes inhibition throughout the brain -> opposite of Glutamate ○ When its released, attaches to dendrite, goes to receptor, and reduces amount of electrical activity in the next neuron ○ Brain has natural way of GABA and Glutamate working together because you can't have too much of 1 they need to balance each other ○ Lacking GABA can give you tremors, loss of motor control because you have too much Glutamate ○ Can change personality because have excessive Glutamate can make you overly emotional, aroused, etc. ○ Too little in the temporal lobe is associated with epilepsy ○ If you take external drug that functions as GABA (ecstasy) low doses can create feelings of euphoria (good) and increases sociability Higher doses can be dangerous, drugs associated with GABA function are used as date-rape drug --> victims feel groggy quickly, impairs their ability to form memory during period 3. Acetylcholine ○ Excitatory, supports memory formation processes, associated with muscle control ○ Black widow spider venom works through Acetylcholine --> enhances acetylcholine related muscle activity (can cause muscle contractions, convulsions and death) ○ The function of acetylcholine is associated with Alzheimer's - disease based age related changes Loosing cognitive functions - think problem solve and memory ○ Involved in REM sleep - rapid eye movement Where body can't move but mind is essentially awake - acetylcholine supporting this activity ○ Botox works through acetylcholine based muscle excitation - attempt to frown but botox in forehead = won't work 4. Serotonin ○ Inhibitory, widely spread throughout brain ○ Associated with psychological experiences captured by pleasure and pain (mood, arousal, sex drive, sleep, eating) ○ Low levels associated with depression - SSRIs , drug used to treat depression increases serotonin functions  ○ Associated with alterations in ability to sleep and eating (too much or too little) 5. Norepinephrine ○ Can be excitatory or inhibitory, found throughout much of brain ○ Supports learning and memory, associated with arousal and eating behaviours ○ Also associated with depression (if too little) , stress or panic as result of too much -> over aroused ○ Works through sympathetic nervous system -> influences arousal, increased heart rate, 6. Dopamine ○ Can be excitatory or inhibitory ○ Strongly known for experience of pleasure, emotional experiences/arousal and motivation ○ Supports learning and voluntary movement ○ Too little dopamine -> depression ○ Too much -> in certain parts of brain are associated with symptoms of schizophrenia ○ Parkinsons disease (older people) -> deficits in dopamine levels ○ Strongly associated with reward mechanisms in brain - commonly identified as being involved in addiction process External drugs that effect dopamine system (crack, cocaine) works through dopamine system and can promote addiction process If you take external drugs It can alter neurotransmitters in 2 ways: 1. Agonist - Enhance NT activity ○ Make NT work more effectively/imitate them - how?: 1. Increase creation or production of NT, storage of it, or release of it 2. External drugs structurally looks like the NT, therefore taking it hooks up with dendrite with same NT (cocaine structurally similar to dopamine so can connect to NT receptors to create dopamine like functions) 3. To interfere with biological systems that normally shut down the NT - systems that prevent dopamine to go out of control (reuptake) the external drug interferes with that process to effectively block slowing/shutting down to allow dopamine to go insane 1. Antagonist - Interfere with NT 1. Can decrease NT synthesis (production), storage or release --> opposite of agonist role  2. When attaches to dopamine receptors, it doesn't act as dopamine, it just blocks dopamine from getting access to dendrite - wouldn't imitate, just blocks Like musical chairs, NT misses out on attaching to receptor Larger Brain Structures and Functions 4 lobes of Brain: 1. Frontal lobe ○ Front of head above eyes ○ Smell, speech, concentration, planning problem solving, motor control 2. Temporal lobe ○ Beside ears ○ Hearing and facial recognition 3. Occipital lobe ○ Bottom ack of head, involved in visual processing 4. Parietal lobe ○ Top back of head ○ Touch and pressure, taste The Cerebrum The cortex is layers of densely packed cells divided in 4 lobes ○ Some degree of localization of function Cerebellum - bottom underneath of brain important for coordination Primary Motor Cortex (strip) Infront of the central sulcus, part of frontal cortex Different sections of the strip of cortex associated with specific parts of brain A lot of neuro real estate for lip movement Yellow has quite large section of motor cortex for hand and digits (fingers) Parietal cortex (behind central sulcus instead of Infront) is sommato sensory cortex which has body map Sensori-motor has body specific representation Cerebellum (CB) Primarily grey matter set of neurons, not many white matter glial cells or myelin so they communicate/process information locally Primary function: ensure timing and coordination of movements ○ Involved in fine tune rapid complex processing that allows you to move fluidly, it's automatic  Cerebellum was always thought to be very simplistic (evoluntionarily old) Alcohol disrupts physical coordination, alcohol directly affects the cerebellum ○ Drinking a lot -> clumsy , Damage to cerebellum affects physical coordination - Case Study Ed had tumour in cerebellum - gradually worsened his ability to walk, removing tumour Prefrontal Cortex (PFC) Newer part of cortex (evolved much later) Infront of motor cortex Most commonly associated with executive functions ○ Processes that focus on controlling short sighted behaviour to be able to act with a goal in mind Ex. Self control, planning, decision making, problem solving, etc Cannot yet specifically assign specific roles to PFC subregions ○ No absolute clear localization of functions, It works in conjunction with different parts of brain PFC receives sensory Info, uses it to plan responses, then communicates with other parts of brain to enact a response Violent murders & PFC - impaired impulse control ○ 41 murderers pleaded non guilty, lost touch of reality not in control ○ Went through PFC imaging machine while doing tasks to determine how active PFC was ○ Found the subjects showed much lower levels of PFC activity than control groups Abnormal levels of pre frontal activation - could have contributed to their murders because no impulse control, no good judgement (all impulsive no planning, all rage murders) Split- Brain effects - Hemispheric Specialization Cortex is divided in 2 -> left and right hemisphere Bundle of white matter nerve fibres called corpus callosum (CC) primarily connect the 2 hemispheres ○ With impact on affected corpus callosum, activity in right motor cortex it gets communicated with left ○ The 2 hemispheres have parallel brain regions, the CC helps them communicate rapidly The different hemispheres have some degree of specialization: hemispheric lateralization of function  ○ Left hemisphere maybe good at processing one type of info, right good at another type of info ○ One more dominant than the other Hemispheric Lateralization of Function Left hemisphere: considered primary language processing center ○ Communicating, reading, writing sentences, forming ideas ○ In the vast majority of right handed people the dominance is in left hemisphere Right hemisphere: dominance in spatial-visual processing abilities (art), facial recognition, music processing Motors and visual systems are contralaterally controlled --> left hemisphere controls right side of body, right hemisphere controls left side of body ○ Information coming from right side of body processed in left hemisphere Cutting of corpus callosum (connection) happened to prevent epileptic attacks ○ Stops electrical activity spread from one hemisphere to the other, stopping seizures ○ Affected perception and memory but a lot of other functions remained intact Case Study: They cut Joes corpus callosum When joe focused on point, everything to right of point goes to left brain: dominant hemisphere for language and speech When word appeared to left of point, it goes to disconnected right half of brain ○ Joe is unable to name it but he can draw it with his left hand because left hand gets major control from right half brain Face Recognition and Prosopagnosia Prosopagnosia --> deficit or inability to link face perception to identity (face blindness) See face/person but don't recognize who it is This could be possible if the face is being looked at as parts/pieces, not as holistic Involves a very specific brain region --> Fusiform face Area ○ Section of Fusiform gyrus associated with house detection, object detection, some get activated when looking at written words, and the FFA associated with rapid detection and experience 2 causal explanations for face blindness: 1. Genetic Possibly given weaker FFA area (brain region) , not effective, limitations in understanding ○ Developmental form of prosopagnosia 1. Damage to FFA Can be from stroke or injury can damage FFA Super Face Recognizers Can be exceptionally good at linking faces with personal identity 4 super recognizers: 1. C.S - 26 year old ○ No matter how much time passes she'll recall face, only happens with faces 2. C.L - 40 3. J.J - 36 4. M.R -31 male All have easily recognized people who have underwent physical changes after long years of not seeing them All use describing strong language Structure of face override smaller insignificant features, helps to remember face & identity Study 1: 25 typical and 4 super recogs ○ 2 diff measures of face recognition: before they were famous & cambridge short memory test (trained on 1 picture looking 1 direction, tested on set of faces and picking which face did you already learn) ○ Findings showed consistent individual differences in face recognition you did well on both tests ○ 2nd study showed face recognition perception - took away requirement of memory (perceptual path) 3 people with prosopagnosia (face blindness) Prosopagnosia has strong genetic links - mother and son didn't recognize each other To try to overcome it Carol repeats the persons name, verbally describe what they look like, Lucy - draws one face everyday but it doesn't help her Capgras Syndrome - Imposter syndrome/doppelganger Neurological disorder (focused area of brain damage) where people start to not recognize people close to them No longer believe the person they're looking at is who they say they are and what they look like They have excellent face recog, they know the person looks like their brother but is calling them a doppelganger Patients cope differently with this syndrome - they just accept this new person is the person's replacement  ○ Patients are usually sad the person they're looking for is now gone, and usually accuse the doppel ganger of murdering the actual person Patient cannot believe the person they see is the person they know 1910 Clifford Beers developed Capgras Syndrome ○ He overcame it - first case ever of Capgras syndrome ○ Wrote about psychosis he endured - can't tell difference between whats in head vs whats real ○ For 2 years he refused to speak to his family thinking they were doppelgangers ○ He wrote a letter to the brother to use as proof when meeting him again that he was infact his brother ○ Cliffords brothers doppelganger gave Clifford the letter and he believed that he was his brother With this syndrome the fusiform face area is working fine (underside of temporal lobe/facial recognition) and amygdala working fine (associated with emotional responses) ○ face recognition is excellent, no identity issues, they know who face should belong to ○ When they see the face they don't feel emotional response you'd expect People with this syndrome see people they recognize but feel nothing so conclude it’s a doppelganger, you can't really be the real person - why?: ○ The connection between the fusiform and the amygdala has been broken -> no connection between face recognition and emotional processing Ted Talk video (to 9:20) Says self awareness is holy grail of neuroscience/neurology Looking at one damaged part of brain with other function being preserved is one way to look at stuff ○ Helps map what part is mediating that function Capgras Syndrome ○ Fusiform gyrus - face area in brain -> when damaged you can't recognize peoples faces Capgras delusion ○ Patient whos completely normal has a head injury, comes out of coma, sees someone they recognize but says the person is an imposter ○ Freuidian view -> when boys are young baby they have strong attraction to mother (Oedipus complex of Freuid) - Amygdala gages emotional significance of what you're looking at ○ If amygdala is excited, heart beats fast, sweating  Doesn't apply if patient was to hear their mom (they think is an imposter) talking to them on the phone ○ They hear her and know it’s the mom but when they see her they say who are you - why:? ○ There is a separate pathway going from hearing centres of brain to emotional centers and this hasn't been cut - therefore through the phone its fine, but visually its an imposter