BBB Midterm 3 Study Guide PDF

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A study guide for the third midterm....

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BBB Midterm 3 Study Guide Emails: [email protected] - language [email protected] - vision and plasticity [email protected] - sleep, motor systems, mental health -

Possible exam questions - Difference between LTP and LTD - Lesion on one place - what would happen - Knowing which layer of a cat’s binocular vision - Don’t need to remember what the critical period is for vision development with ocular deprivation (monocular vs. binocular) - When you have a lesion in the medial temporal lobe, you might have trouble making new memories or consolidating them (focus on this over the specific pathways) - What happens when your circadian rhythm is messed up - what happens with lesions in SCN, etc. and anomalies - EEG recording and seeing the difference between REM and slow wave sleep - Broca’s aphasia vs. Wernicke’s aphasia and their symptoms - telling the difference - If something is in your left visual field or left hand, how might it relate to language, etc. - Understand peptides and neurotransmitters - Orexins and sleep - ACh - Dopamine - Reward and hypothalamus - Parkinsons - Obesity - Glutamate, GABA, etc. - What’s excitatory, inhibitory - Know the Morris Water Maze - Leptin - high and low - how does that relate to AGRP, increase or decrease feeding behavior, and how the systems regulate each other - NPY, AGRP, - stimulate feeding; CART, aMSH - inhibit feeding - Directional tuning graph - Adenosine - important to know - sleep promoting transmitter - Forced swim test and dog cage thing, also maternal care model - Patient HM and the different tests you can give someone to determine where the lesion is based on declarative vs. nondeclarative memory - Anterograde vs. retrograde amnesia

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2 major kinds of glutamatergic receptors - AMPA and NMDA receptors Don’t worry about hippocampal circuitry as much (it’ll be on the exam, but not really that much) - Know its functions and ways to test its function - Morris Water Maze, etc. - Detailed circuitry is not important - Be able to draw direction vectors - CLK and CYC - understand it! Important! Questions - Flip flop model of sleep - Orexin promotes wake - live activatin of LCF - Inhibiting orexin is promoting sleep through VLPO - Influenced by circadian rhythms - light affect on VLPO (maybe) - Grid cells - Specific neurons will fire when you’re at a specific location on the grid - They will fire at spaced out locations that help you build a map of where you are - CREB is related to gene transcription and leads to long term changes for memory - they compare this to short term memory which is related to CamKII and kinase activation - Gene expression and post synaptic changes that lead to long-term memory - Head direction cells - They help with navigation - when an animal is trying to go through a maze, it helps it understand where its body is in relation to its environment - a certain cell will fire when its head is straight versus when it’s facing to the left or right - Dependent on clues in its environment - Relational - not a compass - Monocular and binocular deprivation - Most cells are binocular, but one eye has dominant control over a certain cell - The eye that is open and working gets all the synapses and neurons - When your eye is closed, the neurons that previously worked for the other eye start working more for the other eye - use it or lose it - What? - Addition of AMPA receptors in membrane - Plasticity - NMDA receptors increase and you can phosphorylate channels or - Adding more receptors vs. repression/taking away receptors = plasticity vs. weakening - Calcium and kinases - Remember CamKII

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Calcium activates camkII which phosphorylates receptors and makes them more active and it also does something else which results in potentiation and strengthened synapses which leads to long term plasticity LTP is synapse specific - Another synapse on the same neuron won’t get the same potentiation that another does Answers - Strabismus and alternating deprivation are both B because there is no input for both eyes so there is no binocular vision - to get binocular cells you have to be using both eyes at the same time - Can’t use both eyes at the same time, but alternates - D - don’t have input from one of the eyes, so it looks like h=that - Normal is C - Binocular deprivation is A because you still have the columns, but they’re not really that developed - The ocular dominance columns are still there because of spontaneous activity in the synapses - not based on experience SRRIs - Block reuptake of serotonin into the cell - Depression and anxiety - you need to increase serotonin in the synapse so you decrease reuptake so it stays longer in the synapse Climbing fibers vs. parallel fibers - Parallel fibers = convey sensory information- carry low brain sensory information (I think) - Where your body is - Climbing fibers = indicate motor error - Activate one single purkinje cell when there’s been an error Cortisol - Lower cortisol levels = a feeling of less stress = people with anxiety have too much cortisol - The hippocampus has a lot of cortisol receptors so a lesion in it will result in a long term stress response because there is no uptake of the cortisol Hypothalamic control of posterior vs. anterior pituitary - ??? - Also know about the HPA Axis - Also know about CRH - Negative feedback of HPA Axis Schizophrenia - Different types of symptoms - Positive - hallucination, delusions, paranoia - Negative - low motivation, low emotion, low social functioning

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- Cognitive symptoms - impaired memory, certain tasks - Treatments - Antipsychotic drugs - Biological mechanisms - Dopamine being too high = cause schizophrenia - Medicine inhibit dopamine - Glutamate - patients with schizophrenia have low levels of glutamate receptors Pathways of spinal cord - Understanding what is excitatory vs. inhibitory in said pathway - Indirect and direct pathway - Motor up vs. motor down pathway - Globus pallidus external vs. internal - Don’t need to know the indirect pathway or anything Sympathetic and parasympathetic nervous system - Sympathetic = fight or flight - Uses ACh to synapse on ganglion cells and achieves it effects with NE - Synapses on and affects the thoracolumbar - Parasympathetic = rest and digest - Only uses ACh - Synapses on and affects the craniosacral regions PER and TIM - Gene gets transcribed into mRNA where it leaves nucleus and gets translated into proteins - they then dimerize and go back into nucleus and gets turned into transcription factors that turn off that cycle - Understanding transcription and translation REM vs. non-REM sleep - Short amplitude and high frequency for REM sleep - looks like wakefulness - High amplitude and slow wave sleep for non-REM Language - Primarily in the left hemisphere - With split brain patients after epilepsy - present things to different visual fields and it will only go to opposite side of the brain - Right hand, they can talk about it bc it goes to the left side of the brain - Left hand, right hemisphere, they will say “I don’t know what that is” - Being able to identify something with language or not - left hemisphere vs. right

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Spatial memory - The Morris Water Maze! - Lesion and how that changes their learning Competition vs. cooperation w/ ocular dominance columns - Ocular dominance columns only have so much space, so fibers coming from the same eye work together, but they also fight for space from the fiber from the other eye - Fighting for space in this one region - Decides whether synapses get strengthened or weakened - When they work at the same time in cooperation, they become stronger and take up more space - When they are not firing in sync and there are less string, they prune and fade away, losing space Hebb’s Rule - If things are working together, they will have a stronger synapse Theories of emotion - two of them - James-Lange Theory - You see something scary, perceive it, then visceral reaction, and then interpretation - My heart is racing, I must be afraid - Physiological response happens first - Cannon-Bard Theory - You perceive stimuli, you say I see a snake, I’m afraid, and that kickstarts the physiological response - Combination of both - we don’t know for sure Cortical maps - They can change over time - Cortical map, if you lose an eye, neurons around that part of the brain start expanding and filling it in like ocular dominance - Represents plasticity - Intrinsic horizontal connections - When you stop using inputs from that area, other neurons will fill in the gaps because there is no competition - Growth from dendritic spines, not new neurons CREB II vs. CREB I - Probably won’t show up on the exam - When CREB is phosphorylated which activates gene transcription which is important for plasticity - When CREB II is bound there is no gene transcription and CREB I is the opposite? - Know that it’s involved in gene transcription - specifically CREB I that

leads to gene transcription -

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LTP LTD -

Taking memories and making them more long Memory consolidation of working memory and short term memory Need long term potentiation

The opposite Pruning away connections that you don’t need anymore In LTD, small amount of depolarization, which leads to a little bit of calcium which takes away some receptors and makes the synapse less strong - Dephosphorylation AMPA receptors so they become less active - They do this instead of phosphorylating them - Some small depolarization vs. LTP which is huge depolarization LTP in CA1 - A CA1 neuron; whether you stimulate inputs on left or right - Tetanus stimulus a bunch of times - After tetanus and stimulated a bunch, there is a higher depolarization - When not stimulated, there is no LTP - LTP is specific to the inputs that were stimulated NMDA receptors - What is responsible for LTP - If you add APV, which blocks NMDA receptors, even after really hard tetanic stimulation, you don’t see LTP - Ligand and voltage gated - Cell needs to be depolarized and there also has to be glutamate to bind the receptors so that magnesium that’s blocking the channel can leave - then there is an influx of calcium through the channel which leads to activation of CREB in gene expression, forming CamKII which leads to recruitment of AMPA receptors to emembrane which leads to strengthening of synapse Purkinje cells - A cell is designed to keep your eye open and there are parallel fibers that bring in sensory information - A beat is playing and at the same time they blow air into your eyes - reflex is close eyes - Motor learning is when you hear the beat, you close your eyes before the air ever comes - motor contitioning - Purkinje cells are meant to keep the eye open - Parallel fibers connect with purkinje cells, relaying weak sensory information - Climbing fibers profuse innervation to a purkinje cell to show an

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error and weaken the strength of the synapse - This tells you to keep your eye closed Directional tuning graph - Cell firing more with movement in one direction vs. the other (left vs. right) - Most firing will happen at the preferred direction - Directional tuning curve of upper motor neuron in M1 - Preferred direction is the biggest vector, smaller for non preferred direction - then it sums up to be a population vector Anxiety disorders and tehri drugs - Benzodiazepines increase GABA which is an inhibitory neurotransmitter - Too much activity in amygdala = anxiousness - Reduces this and suppresses it in your circuitry - GABA reduces anxiety - Too much activation = extra activity, so GABA inhibits this activity and calms things down - Benzodiazepines are xanax and valium - bind on binding site of GABA site and acts as agonist so it increases GABA signaling - more GABA to reduce anxiety effect Adenosine - important to know - sleep promoting transmitter - How coffee works - Caffeine blocks adenosine receptors - antagonist that blocks adenosine receptors and makes you feel more awake Sleep - Less synapses when sleeping - Strengthening synapses and pruning the ones that are white noise - Dendritic spines Forced swim test - The more time the mouse swims, the less depressed - More time immobile = depressive phenotype - Same with dog and learned helplessness - dog staying in box and shocking - treated with antidepressants, it moves - Action vs. inaction - Used as phenotypes for depression and get better when treated with antidepressants - Forced swim is a stress model - Morris Water Maze is involving memory - Maternal care model - how babies are treated in early life - more touch - Increased maternal care is protective in future stress response - More licking and grooming - More stress receptors? In hippocampus

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Circadian rhythm - SCN, VLPO, etc. - Pacemaker - Zeitgebers lead to regulation of SCN which leads to the output (whether you fall asleep or stay awake, etc.) Learning and memory plasticity - Neocortex is the site for long term storage and memory - retrograde amnesia - Consolidation - Hippocampus is the site for forming new memories - anterograde amnesia LTP - Kinases that are NMDA active and have to do with Ca2+ levels - 2 major kinds of glutamatergic receptors - AMPA and NMDA receptors - Similarity between them - Both bind glutamate - Differences - AMPA open really quickly and there is immediate depolarization - NNMDA is slower in opening - To open, AMPA needs glutamate - ligand-gated channel - NMDA needs glutamate AND needs the postsynaptic membrane to have a baseline depolarization because magnesium is in the pore that blocks it - Magnesium is a positively charged cation so to push it out of the receptor, the positive charge from the depolarization in the cell will repel magnesium - It requires both the pre and postsynaptic membrane to be active at the same time - Coincidence detector!! Happens at the same time - If they fire together, NMDA can come in and facilitate these changes - To get vesicle fusion, you need calcium to enter the presynaptic neuron - As a result of vesicle fusion, glutamate is released - Diffuses across the synaptic cleft and the transmitter is gonna bind receptors AMPA and NMDA - When AMPA opens, Na+ flows in to depolarize the cell - Then, as a result of the depolarization, then the NMDA receptor channel can open and bind to glutamate - AMPA and NMDA receptors usually come together at a synapse

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NMDA opens and there is a Ca2+ influx - Passes calcium, while AMPA does not pass calcium - So now, we’re in a high calcium state and it activates kinases which allows for LTP - CamKII is a kinase and kinases phosphorylate things - CamKII phosphorylates CREB, which activates it so that it can make gene expression changes - LTP happens as a result - Plays a role in learning and memory, but also on development - LTP, long term potentiation, is the patterns of synaptic activity that produce a long-lasting increase in signal transmission between two neurons - Changes in gene expression = long term Short term plasticity - STP - Same thing but not enough activation for changes in gene expression - The calcium also phosphorylates the receptors which stabilizes the receptors in the membrane and possibly making more receptors be pushed up into the membrane, which makes them more effective slightly - Temporary change - It’s temporary because phosphorylating something is easily reversible because something can come and take the phosphate right off - LTP is long term because the changes in gene expression lead to making certain protein and that can’t just be changed - Proteins allow the synapse to be more active LTD - long term depression - weaker synapse - When you forget something, you use the synapse less and it’s LTD kind of - Low calcium, so less NMDA receptors active - This low calcium state is affiliated with LTD - NMDA receptor increase is related with shift from LTD to LTP - IMPORTANT - There are phosphatases that take away phosphates that are bound to things which makes other receptors less stable and breaks the strength of the synapse Synaptic homeostasis hypothesis - Net increase in synaptic strength throughout the day (a lot of LTP during the day) - During sleep, you get rid of and prune away some of this stuff so you can pick up on what was important during the day - Decrease synaptic strength (LTD) - Potentiation of things when you’re active and learning, so

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depression when asleep Ocular dominance columns - If you inject one eye with radioactive stuff, you can see the dominance of that one eye (the columns) - In layer 4C of V1, in a normal state, there is only monocular inputs - either right eye or left eye - Two columns on the left and right - Layer 4C sends information above and below and information starts to coverage from both eyes - Stereopsis = depth perception - need two eyes - In the cortex, there are cells that respond to right eye, left eye, and a gradient that respond to both, one more than the other - Bars on the chart - Middle bar responds equally to both - When one eye is covered, no normal distribution and most of the cells shift in activity towards the open eye - This happens within the striate cortex - Retinal and LGN cells are okay, not striate cortex - When you cover one eye really early on, the columns shift, but totally normal development when you do this too late - Critical period - The time when the brain is most plastic - Really receptive to stimuli - In layer 4C, monocular, and in other parts of the cortex, it’s binocular normally!!! - pay attention to which part of the cortex! - If you cover both eyes, the dominance columns look the same, but weaker - because of spontaneous firing that occurs - This told us that, because one is not getting more attention than the other, it looks more normal - The brain operates on competition and whether one is more active than the other - If you put a patch on one eye and then the other (both eyes can;t work at the same time) then you lose binocular vision - cells that only respond to contralateral or ipsilateral eye - monocular vision has extended out into the cortex - The gradient in between does not work - Would not have depth perception - This is alternating deprivation - In all layers of cortex besides 4C Direction vectors - What would the movement look like as a result of a summating a direction

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vector - big in the motor vector Monoamine hypothesis - SSRIs are one of the few things that work, but only work for 50% of the people that take them for depressed and anxious people - They take a few weeks after your brain dealing with more serotonin around - If serotonin is keeping the hypothalamus in check, the hypothalamus also keeps the serotonin in check, which is why it takes so long to work Circadian control - Endogenous - on and off activity within that is entrained by external cues, zeitgebers - Self-sustaining - endogenous to you - 24 hour rhythm, but there are other categories of rhythms - Uktradian (less than a day - breathing), infradian (many days - periods), circannual (months in a year - mating behavior) - SCN is getting direct information from the retina about whether it’s light or dark outside to entrain this rhythm that exists - The SCN is an oscillator itself and has its own rhythm Arcuate fasciculus - The white matter tract that connects Wernicke’s and Broaca’s Areas won’t have a problem with comprehension or production, but the combination of the two - Like repeating words that you hear!!, and also sometimes answering a question, etc. The Wada Test - Anesthetize one half of the brain (carotid artery) - this told us that most language production happens in the left side of the brain - This is also is used for brain surgeries Place cells and grid ...