Final Study Guide - Behavioral Neuroscience
Final Study Guide - Behavioral Neuroscience PSYC 4183-001
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Date Created: 05/06/16
Final Study Guide - Behavioral Neuroscience 1. Hearing a. Stimulus b. Sensory Apparatus c. Neural Pathways d. Cortical representations i. A1 2. Motor System a. Neural Pathways b. Cortical representations i. M1 ii. PMA/SMA iii. Basal ganglia iv. cerebellum 3. Learning & Memory a. Cellular Mechanisms of Learning i. Long Term Potentiation (+hippocampus LTP) 1. Glutamate Receptor (AMPA, NMDA) b. Neural Circuitry of memory i. Medial Temporal Lobe/Hippocampus ii. Basal Ganglia iii. Explicit memory & Implicit Memory Understand the structure and mechanisms of the inner ear. Base V. Apex of Basilar membrane Memorize the complete auditory pathway and where it decussates What is the significance of the superior olive? What are the functions of the 2 streams of A1? How does damage at different points in the auditory pathway affect hearing? Structures of the Inner Ear and their functions Know the descending pathways of the motor system Know M1 organization and encoding mechanism Function of PMA/SMA, Basal Ganglia, & Cerbellum Understand LTP, the role of the glutamate receptors and how APV affects LTP What is the Delayed non matching Sample task? How does it work? What does it measure? What is the Morris Water Maze? What does it measure? Implicit V. Explicit memory Know the function of the 3 most critical regions of the limbic system and how damage affects them What are the pathways of the lateral nucleus and their importance? How did lobotomy affect behavior? What are the different forms of aggression and how were they stimulated? 1. Hearing a. Stimulus: Sound Dimensions of Sound 1. Amplitude (Loudness) a. Greater pressure = Greater amplitude= louder b. Amplitide = height of waves (image ) 2. Frequency (Pitch) a. How close together the vibrations are b. Smaller wavelengths = smaller pitch, larger wavelengths = larger pitch c. Wavelengths = distance between waves 3. Complexity (Timbre) a. Multiple frequencies with a base frequency creates a complex sound b. How fast a sound ramps up or is created is affected by complexity c. Being able to tell the difference between a note on the piano or the guitar is due to complexity A mplitude L oudness **REMEMBER: Amy Frequently Collects Little Purple Tins Frequency P itch Complexity T imbre b. The Sensory Apparatus Anatomy Pinna – Allows you to localize sound Auditory canal – brings sounds in which bands on the eardrum Eardrum - vibrates at the same frequency as the sound and transfers it to ossicles Cochlea: Spiral shaped structure where all transduction of sound occurs -Filled with fluid which poses an issue since sound is vibrations through the air - Eardrum counters this by transferring the vibrations from a large surface area through the ossicles to the small surface area of the oval window This condenses the sound so that way it can go through the cochlea a smaller surface area INCREASES the pressure which is what allows the signals to go through the denser cochlea Semicircular canals: Involved in vestibular sense (filled with fluids) Inner Ear Cochlear Structures 1. Basilar membrame- membrane upon which the organ of corti is situated a. Lines all of the cochlea Deeper look at the Basilar membrane -It is tapered in width so that it is wider at the apex of the cochlea than at the base -This causes a difference in what part of the basilar membrane is being agitated the most by different frequency sounds The base is moved more by high frequency sounds The apex is moved more by low frequency sounds **Another way to explain it : Sound causes the stapes to move in and out which in turn causes fluid within the cochlea to flow. This generates a travelling wave within the basilar membrane. The region of the basilar membrane deformed by sound is dependent on the sound’s frequency. The neurons along the basilar membrane is what codes these sounds and are set for high or low frequency based off their location in the basilar membrane 2. Organ of Corti: Sensory organ that contains auditory hair cells (contains mechanoreceptors) a. Continuous along the entire basilar membrane b. Vibrations of these hair cells is what turns into neural code Deeper look at thOrgan of Corti - Has outer hair cells and inner cells o Inner hair cells: transduce sound by responding to perturbations of the basilar membrane. o Outer hair cells: act as an amplifier pushes against the tectorial membrane to create greater graded potential for the innerhair cells tectorial and outer hair cells push back and forth to AMPLIFY the vibration and thus stimulate the inner hair cells (depolarizes it) 3. Tectorial Membrane: Membrane above the organ of Corti. Hair cells move against this membrane a. Means of helping the mechanoreceptors so they have something to be flexed/pushed against aids in transduction c. Neural Pathway =Mostly contralateral organization but not completely - This is because we have to figure out where sound is arising from (localizing) - In order to localize better you need to combine sound from both ears Left cochlea auditory nerve Left Cochlear Nuclei = Partially decussates to the contralateral side and some decussates to the ipsilateral side Superior Olive Superior Olive: First structure in the auditory pathway to receive binaural inputs - Anything damaged AFTER the superior olive will not necessarily cause total loss of hearing from that side (because it is ipsilateral up until the superior olive) - Uses interaural time differences and interaural intensity differences to figure out where a sound is coming from o Interaural Time Differences: Difference in arrival time of sound between the two ears Allows localization in the horizontal plane (either side of your head/ across) o Interaural Intensity Differences: Difference in sound intensity between the two ears Allows localization in the horizontal plane o Pinnae Cues: Difference in sound patterns caused by filtering by the pinnae Allows localization in the vertical plane (high above or below you) ** if you put silly putty on you pinnae to smooth out all the fold you would have trouble locating sources of sound on the vertical plane because your brain is used to the pattern of echoes for your unique pinnae folds (AKA the patterns and source identification is LEARNED) **After passing through the superiorolive the spatial information feeds into the Inferior colliculus which contains a complete map of auditory Space d. Cortical Representations i. Primary Auditory cortex = A1= the core Tonotopic/Cochleotopic organization: Orderly layout of frequency along A1 o Anterior A1 = Apex of cochlea low frequency representations (500 Hz) o Posterior A1= Base of cochlea High frequency representation (16,000 Hz) Has SOME Cortical magnification where there is a bit more tissue devoted to representing mid=frequencies A1 Neural Response Properties FrequencySelectivity:Thefrequencythatthecellpreferswillstimulatethatcellmorethan other frequencies Spatial Selectivity: The location of the sound in space will stimulate a cell more in its preferred location than in any other location Has Columnar organization (to an extent) o Frequency Columns o Summation Columns and Suppression columns Provides info about depth in space Summation = columns of cells that are MAXIMALLY responsive to sound from both ears Suppression = responsive to sound in one ear vs. the other Information feed of A1 A1 info belt Parabelt - Belt: Surrounds the A1 - Parabelt: Surrounds the belt *From A1, the information separates into “what” and “where” streams towards the prefrontal cortex Where Stream Infogoingthroughtheparietalcortextendstobespatially related What Stream Info going through T2/T3 tends to be Complex characteristic identifiers - Detects Auditory “objects” A voice o your ability to recognize frequency, timbre, and signaturepatterns iswhatallowsyoutoidentifyavoice’suniqueness HOWEVER, Wernicke’s area: Critical for language comprehension & understanding speech this argues that not EVERYTHING object oriented goes ventrally/anteriorly in the pathway 2. Motor System a. Neural Pathways Posterior Parietal cortex/ Brodman area 7 – visually guided movements o Also contributes to the planning of motor output Prefrontal cortex – Goal directed behaviors o Contributes to motor output that helps you achieve that goal Descending Pathways - Activity within all descending pathways is modulated by cortical motor areas Lateral Pathways : axons traveling down the lateral side of the spinal cord - Involved in voluntary movement of the disal musculature - under direct cortical control - Largest concentration of cell bodies for these pathways are located in the Primary motor cortex 1. Corticospinal tract : 1 cell body, 1 axon that goes all the way down to the motor neurons in the spinal cord a. Motor neurons = cell bodies in the ventral root of the spinal cord b. Completely contralateral (stroke in the left motor cortex paralysis on the right side) c. If you suffer a stroke in this pathway it is possible to have the pathway rerouted to the red nucleus of the midbrain to continue through the rubrospinal tract (via plasticity) i. Damage could potentially cause paralysis but if the rubrospinal tract is still intact then you could potentially recover 2. Rubrospinal tract: Smaller, originates in the red nucleus in the membrane a. Completely Contralateral b. Damage of this tract in monkeys caused temporary deficits in motor movements but you can recover this tract is thought to have a role in movements for early development (i.e.crawling) Ventromedial pathways - Receives inputs from the Primary motor cortex - Involved in the control of posture and locomotion Allows you to keep the tone of musculature and balance - You don’t have to actively think about this control its how you stay standing or sitting upright without thinking about contracting/tensing your muscles 1. Colliculospinal tract: Projects into all the other pathways (listed below + rubrospinal tract) 2. Vestibulospinal tract: Corrects when your head suddenly accelerates AKA you lose balance/fall in a direction a. Coordinates information to keep you uprught 3. Pontine reticulospinal tract 4. Medullary reticulospinal tract a. Subserves orientation (automated) b. Cortical Motor Representations Plan it in PMA/SMA execute it with M1 M1 receives additional info from Basal Ganglia and Cerevellum M1 Primary Motor Cortex = M1 - Provides majority of descending fibers in the corticospinal tract o Placing an electrode on the M1 and stimulating it will send a signal down the corticospinal tract o Damage can lead to partial or full paralysis - Cell bodies in M1 have axons that descend all the way down the spinal cord o Sometimes thought of as an extension of the spinal cord in terms of function - Last stage before you can actually contract musculature Organization - CONTRALATERAL - Somatotopic organization: Neighboring regions of M1 control the musculature of neighboring parts of the body o EX: Neurons that move your thumb will be found next to the neurons that move your forefinger - Cortical Magnification: Larger portions of the M1 is devoted to the more dexterous parts of the body o Large portion goes to face and fingers lips and tongue = highly dexterous as it produces language Encoding - Neurons in M1 encode for 2 aspects of movement: o Direction o Force - There is a distribution of preffered output in the neurons of M1 o They are TUNED for a direction but that only means the neuron will fire the most for that direction, but it does not move only in that single direction - The only way to accurately predict the exact movement that will occur by stimulation is by looking at a whole population of cells that are stimulated o The Average vector of response in the population of cells will determine the direction of movement *This knowledge has helped in the creation of neural prosthetics/robotic arms (prosthetics controlled by the brain) PMA/SMA - Planning movement, complex sequences of distal musculature in particular - PMA and SMA represent different muscle groups Damage - Damage to just the PMA/SMA does not cause paralysis - Creates more difficulty in planning and executing motor actions Monkey experiment: Instructing a monkey to press a button - When there’s no instruction there is a baseline firing rate in the monkeys brain - When a monkey is given an instruction the PMA starts firing rapidly o This means that there is a motor plan o Instruction stimulus turns on - When the monkey moves according to those instructions the SMA starts firing rapidly o Trigger stimulus comes on o Instruction stimulus turns off Mirror Neurons – can be found in the PMA o Fires when a particular movement is performed AND when the monkey sees a similar action being performed by someone else (i.e. the human trainer) o Thought to represent learning through imitation (monkey see, monkey do) - Visually observing what someone else is doing converting that into a program of how it was done and translating it to your own body and then executing that same action. Basal Ganglia - Involved in the selection and initiation of voluntary movements - Receives widespread inputs from the cortex, process that information, then feed it back into PMA/SMA through the thalamus (Ventral Lateral Nucleus) - This cycle of info. proccessing through the basal ganglia is referred to as the cortico-basal ganglia motor loop Cerebellum - The cerebellum is involved in timing and coordinating sequences of movements - Forms another motor loop with cortex, the corticocerebellar motor loop, which mediates the coordination of movement sequences. - Broad cortical inputs feed into the cerebellum then project back into M1 via the VL nucleus of the thalamus. 3. Learning & Memory a. Cellular Mechanisms of Learning Eye Blink Conditioning = Neural model of Classical conditioning (think Pavlov’s dog) - Puffing air at the eye is met with a reflexive blink response - By pairing a tone with the puff of air you can create a synapse between the neuron in the auditory system (of that tone) to the neuron that causes you to blink o Eventually you could cause that person to blink reflexively to that tone even without that puff of air THEREFORE, The strengthening of a synapse = learning If you continued to CO-ACTIVATE the “blink” neuron with the other two neurons you will begin to see GROWTH of dendrites in the “blink” neuron that will connect to Synapse T (in image) and thus we see the STRENGTHENING of that synapse - Learning in the brain is activity dependent Hebb’s Rule: A synapse is strengthened by the simultaneous activation of presynaptic and postsynaptic neurons o Cells that fire together, wire together i. Long Term Potentiation (LTP) = Cell Learning *LTP enhances the effectiveness of synaptic transmission via strengthening of synapses (as explained in the eye blink conditioning example) - LTP= The most simplistic representation of Learning in the nervous system - Requires 2 events: The activation of synapses and depolarization of the postsynaptic neuron - LTP can also lead to the formation of new synapses dendritic spines 1. Glutamate Receptors : post synaptic glutamate receptors are KEY to LTP - NMDA: Detects correlated activity o Ionotropic, Ca++ o Induces learning via Calcium (Ca++) - AMPA: Strengthens a synaose o Ionotropic; Na+ o ‘Keeps’ the learning there NMDA - Detect’s the co-activation of the presynaptic and post synaptic neurons o The co-activation must occur at a HIGH/significant rate to be detected - Neurotransmitter Gated AND Voltage Gated Channel - NMDA receptor controls Ca++ channels which is normally blocked by Magnesium o You must have a already depolarized post synaptic cell AND glutamate must be released by the presynaptic cell into the synaptic cleft at the SAME TIME to remove Mg++ and unblock the Ca++ channel o This then allows Ca++ to go through the NMDA receptor (green tube in image) AMPA - Increases strength of synapse Entrance of Ca++ from the NMDA receptor causes the activation of protein kinases o The activation of protein kinases Induces LTP in two ways 1. Increases EPSPs of existing AMPA receptors by having larger currents run through them 2. Inserting new AMPA receptors into the postsynaptic membrane a. = more pores that Na+ can go through Bigger EPSPs LTP in the Hippocampus Paired stimulation 1. Paired stimulation leads to LTP - It can make a cell go from generating NO EPSP to generating a LARGE EPSP o This shows that we are set up with the ability to learn 2. High-frequency stimulation induces LTP a. A “brute-force” type of method b. Sends massive amounts of action potentials down a pathway (50-100Hz) ***Experiment: Inducing LTP while using APV to block the NMDA will cause random sizes of EPSP to be released. This shows that NMDA is critical to the learning process. Preventing NMDA = preventing LTP 3. Low-frequency stimulation of hippocampal pathways leads to long-term depression (LTD) a. Lasting reduction in synaptic strength Smaller EPSPs b. Like forgetting due to the weakening of synapses Used in clinics to decrease activity in areas of the brain that are overactive (depressed patients, bipolar patients, etc…) Artificial Neural Networks - Can be trained a lot like brains do - Mimics LTP in a biological neural networks and applies it to artificial neural networks - The most successful way to train computers to SEE things (for example) o Can also be trained to identify any trend in data b. Neural Circuitry Engram – A term used to refer to the neural representation or location of a memory - AKA Memory Trace **Remember! There is not a single place in the brain where a memory resides, it is distributed across the entire brain Explicit memory Medial temporal lobe and especially the hippocampus is important for forming long term memory Although there is no one storage space for memory there are critical structures for laying down that memory Relational Memory Theory: Poses that the hippocampus forms representations of arbitrary relations among the constituent elements of experience Tying a bunch of stimuli, that were together at the same moment in time, together. Medial temporal Lobe/hippocampus - This and structures within the diencephalon are particularly important for the formation of new long-term declarative and spatial memories. Hippocampus: Receives sensory information Via the rhinal cortex Wilder Penfield’s Experimentation on patients with Electrical Stimulation in the Medial temporal lobe: - Found that when he stimulated a patient in the Medial temporal lobe during a surgery it invoked some of the patients memory o However, it is possible that these could have been hallucinations or an untrue memory - Patient H.M. had portions of his medial temporal lobe removed to alleviate epilepsy o Had extreme anterograde amnesia and partial retrograde amnesia for the years preceding the surgery o He had the feeling of being stuck in time Image: Example of H.M.’s surgery results now lacking the medial temporal lobe Retrograde amnesia = when you lose memories from before the brain trauma/death Anterograde amnesia = when you cannot form new memories after a brain trauma death Animal Models **An Animal model of human amnesia can be created through the induction of medial temporal lesions and measuring resultant changes in memory using the: A. Delayed non-matching Sample Task - recognition over time Example: A monkey is given an object to rememberthen a blind fold is placed on the monkey for a length of time= delay meanwhile a different object is placed in front of the monkey, after the blindfold is removed the monkey must identify the different object - This task teaches the monkey to remove the object that does not look like the object they were just looking at previously o Small delay = Seconds – 10 mins o Long delay= 30 min – hours requires it to use its long term memory A normal monkey will more or less remember up to 10 min after In a monkey with a lesioned medial temporal lobe, it will more likely make a mistake as time goes on B. Morris water maze – understanding spatial memory Somewhere in a tub of water there is a little platform right under the surface of the water - Then a rat is placed in the tub, the only way to escape is to get on top of the platform o The faster the rat finds the platform after 10 trials = learning - Rats with hippocampal lesions fail to learn the location of the submerged platform, swimming in a random fashion until they arrive at the platform even after 10 or infinite trials. Place Cells: Specialized cells in rat hippocampus that encode specific spatial locations in the environment o Specific regions light up in the brain depending on where the animal is located (usually in an enclosed space) Human Models ** There is evidence of hippocampal involvement in human spatial learning and memory as well A. Maguire’s study of London Taxi drivers - He found that those who used their hippocampus more had larger hippocampal volume AKA hippocampal growth - Those who were taxi drivers longer had greater volume/growth in the hippocampus B. Maguire’s PET study -Used a navigation task for subjects under a PET scan had to find their way through a virtual world - Findings revealed significant hippocampal activations Implicit Memory Long-term memory of tasks, skills, and procedures that occurs outside of conscious awareness H.M. cannot form new long-term declarative memories but can form new long-term implicit memories Basal Ganglia: Caudate and the Putamen (striatum) play an important role in the formation of implicit memory o Dopaminergic inputs to the striatum are critical for normal function. Parkinson’s patients show significant deficits in implicit memory tasks du to this lack. Rain prediction task (subconscious learning) <-- Image: Implicit memory task involving cards Hippocampal group or those with Anterograde amnesia had improvement in their ability to predict the “weather” with this task although they would have no recollection of the task after some time. This implies that: - They can acquire implicit memory/procedural memory - Motor skills and subconscious learning is still intact - Explicit memory cannot be developed Parkinson’s group did not improve their ability to predict the “weather” even after 50 trials. They were able to still remember all the details of the task just as well as the control group. This implies that: - They cannot develop implicit memory since they could not learn a pattern of sensory visual input - They have good explicit memory Working Memory: Active, short-term store of information. - When you don’t need it, it is gone - Through rehearsal the memory can be kept to transfer it to short-term memory and then eventually to long-term memory Common rule for working memory: 5-9 digits can be stored for a brief time in working memory. “chunking” helps you to remember one, like remembering your own area code in a phone number allows you to chunk 3 digits as one idea. Dorsolateral Prefrontal Cortex (DLPFC) - Made up of several regions of the prefrontal cortex -Crucial for proper working memory function Damage - Damage to DLPFC does not mean you lose or no longer have working memory - Working memory will probably get worse - Theory: Each sensory modality has its own form of working memory; i.e. working memory is a system Emotion Emotions: Subjective feelings accompanied by particular psychological states 3 types of response: - Behavioral - Autonomic - Hormonal Affective Neuroscience: A currently changing field that’s attempting to remove subjectivity of emotional description Limbic System: Network of brain structures involved in representing and expressing emotion 3 Critical structures: - Amygdala - Hypothalamus - Ventromedial prefrontal cortex Other included structures: - Cingulate cortex - Mediodorsal nucleus - Ventral portions of basal ganglia 1. Amygdala = threat processing o Allows one to acquire implicit memory of stimuli that is a threat o Forms phobias due to coincidental association of something as a threat i.e. A rat sees a cat toy and is scared because it is associated with a presence of a cat - Fearful faces evoke an increased response in the amygdala relative to a neutral face o there is NO difference between happy and neutral faces with amygdala activity Kluver – Bucy Syndrome: Bizarre behaviors that occur following a bilateral temporal lobotomy o including a DECREASED fear response (w/ amygdala damage) Focal Bilateral Amygdalae Damage: - causes a deficit in fear response - Patient SM, AM and BG famously have focal bilateral amygdalae damage - They still understand when they are in unfavorable/dangerous situations but will not have an emotional/physiological reaction to these situations **Twins, AM and BG: had a (so far unexplainable) situation where they were given increased carbon dioxide in their bloodstream and ended up experiencing fear! **NOTE: Patient S.M. cannot accurately recognize fearful emotional faces. Fear conditioning with Patient SM versus Control group - Study paired stimulus with pain Fear conditioning Physiological fear responses were measured such as Heart rate and skin conductance (sweaty palms) - Control group: Reacted to their conditioned stimulus with an increase in physiological fear responses - Patient SM: showed NO change in fear response measures with the conditioned stimulus **The first response Rats show is freezing when they see a threat Fear conditioning with rats pairing a beep sound with a shock so that rats learn to fear the beep sound Important Nuclei of the Amygdala: - Lateral Nucleus: Where learning in the amygdala occurs o Damage= equivalent to “forgetting”all your fears - Central Nucleus: takes output from lateral nucleus and triggers other systems to deal with the stimulus/threat o Via fight or flight, or some other physiological response o Damage= gets rid of any response to fear o Get different responses based on where information is sent: 1. Hypothalamus autonomic response 2. periaqueductal gray matter behavioral reaction 3. cerebral cortex emotional experience Lateral Nucleus: - Lateral nucleus receives sensory information from the thalamus and cortex - Fear acquisition is mediated by long- term potentiation (LTP) Fast Pathway-direct input from thalamic nuclei - Helps with survival - Aids in innate fear response Slow pathway-indirect input from cortical sensory areas - This pathway is used to differentiate the more complex stimuli - i.e.: if a rat is conditioned to fear a tone that’s 1000Hz and trained to not fear a 100Hz tone it can discriminate thanks to the cortex o Damage to slow pathway: destroys the ability to discriminate between fine differences 2. Hypothalamus Early studies of aggressions demonstrated that transectioning the forebrain but leaving posterior regions of the hypothalamus intact resulted in sham rage. - Removal of the entire hypothalamus did not induce sham rage Different forms of Aggression Stimulating the medial hypothalamus induces affective aggression Affective Aggression: A response to a threat typically with some form of intimidation (i.e. a cat hissing) Stimulating the lateral hypothalamus induces predatory aggression o linked to hunger and feeding 3. Ventromedial Prefrontal Cortex (vmPFC) Plays an important role in the control of emotional behavior Phineas Gage: Famous patient with injury to vmPFC lower ability to regulate and control emotion In the 1930s frontal lobotomies were used to treat a number of emotional disorders. - Lobotomized patients exhibited blunted affect and a loss of emotional control Those with damage to vmPFC have a more logical approach to decision making than emotion based decision aking Tied to psychopathic tendencies but low correlation Subgenual Cingulate + Depression On average, those with low activity in anterior cingulate cortex is associated with unipolar depression In normal subjects, there is HIGH activity in the anterior cingulate cortex when recalling sad events Example Questions 1: The ossicles are: A. Bones B. Membranes C. Mechanoreceptors 2: A frequency of 20,000 HZ would maximally displace what part of the basilar membrane? 3: Fill in this pathway: CochleaCochlear Nuclei SO ? ? A1 4: True or False. Each superior olive receives input from both the left and right ear. 5: How will hearing be affected with bilateral damage to the inferior colliculus? 6: How will hearing be affected with damage to the left A1? 7: How would bilateral damage to the most posterior portions of A1 affect hearing? 8: A given neurons in M1 will control a single muscle of the body 9: T/F -Damage to the rubrospinal tract in the human will lead to paralysis 10: Which of the following has the largest representation within primary motor cortex. A. Foot B. Stomach C. Hand D. Arm 11: Suppose you are recording from the arm representation of macaque M1 as the monkey performs a motor task moving joystick toward one of five targets (right). Out of the cells from which you are recording, six exhibit significantly increased firing rates and are tuned to preferred direction of 70, 40, 180, 150, 40, and 60 degrees. Which direction will the monkey move its arm? 12: Which of the following best summarizes the result of LTP? A. Smaller EPSPs B. Larger EPSPs C. Smaller action potentials D. Larger action Potentials 13: The ____ receptor is most critical for the induction of LTP A. AMPA B. NMDA C. Kinase D. Kainate 14: What do you suppose will happen if we perform an eye blink conditioning procedure after administering a large dose of APV? 15: Following Bilateral medial temporal damage, monkey performance in a DNMS task a) Will be best at long delays b) Will be best at short delays c) Will not differ from sham monkeys 16: T/F - Hippocampal damage leads primarily to retrograde amnesia 17: What task is often used to test spatial memory in rats? 18: Rats have an innate threat response to the odor of feline urine how will this response change following bilateral damage to the amygdalae? a) The rat will completely lose its sense of smell b) The rat will continue to show a threat response to the odor as this response is not learned c) The rat will no longer show a threat response to odor Example Question Answers 1. A. Bones 2. Base (receives high frequencies) 3. Inferior colliculus Thalamus (MGN) 4. True 5. You would become deaf. This will prevent the auditory information from completing its pathway to the cortex which makes one essentially deaf. 6. You would not become deaf. This is because after the superior olive, the auditory pathway will receive information from both ears on each side of the brain AKA binaural representation. So losing the Left A1 would not cause a complete loss of hearing on either the right of left side of auditory space so you would still have your hearing. 7. You would be unable to hear high frequencies. This is because bilateral damage to Posterior A1 takes out the reception of information from the base of the cochlea in both ears. Base of cochlea = responds to high frequencies. 8. False. A population of M1 neurons signal a set in the spinal cord 9. False 10. C. Hand --> Hand and face are the most represented in the M1 since they require the significant amounts of fine motor control 11. 90 degrees (take the average of the numbers) 12. B. Larger EPSPs 13. NMDA 14. You would NOT get any responses because APV blocks NMDA receptors and causes you to lose the ability for LTP learning AKA it prevents your neurons from learning so therefore they begin forgetting. 15. B 16. FALSE (+retrograde amnesia is fairly uncommon) 17. Morris Water Maze 18. C. the rat will no longer show a threat response to the odor Practice Question Answers 1. False 2. True, procedural memory is intact 3. E. 5 minutes (longer time = worse response) 4. B. fear conditioning will not occur 5. A. A neuron that responds selectively when an animal occupies a particular space location 6. Low frequency 7. Short explanation: (KNOW LTP in and out) influx of ca drives induction of LTP, expression of LTP is through ampification Long Explanation: 1. LTP occurs due to the NMDA and AMPA receptors. NMDA detects the co-activation of the presynaptic and post synaptic neurons, therefore recognizing the correlations. AMPA increases the strength of a synapse. 2. Detailed Process: NMDA receptor controls Ca++ channels which is normally blocked by Magnesium a. You must have a already depolarized post synaptic cell AND glutamate must be released by the presynaptic cell into the synaptic cleft at the SAME TIME to remove Mg++ and unblock the Ca++ channel b. This then allows Ca++ to go through the NMDA receptor c. Entrance of Ca++ from the NMDA receptor causes the activation of protein kinases d. The activation of protein kinases Induces LTP in two ways i. Increases EPSPs of existing AMPA receptors by having larger currents run through them ii. Inserting new AMPA receptors into the postsynaptic membrane 1. = more pores that Na+ can go through Bigger EPSPs 3. How it is induced experimentally in hippocampal slices: Experiments demonstrate that these slices can follow the hebb rule: “cells that fire together, wire together” o Paired stimulation: It can make a cell go from generating NO EPSP to generating a LARGE EPSP o High-frequency stimulation: induces LTP by sending large amounts of action potentials down a pathway 8. Weather prediction task: PArkinsons patients vs. Hippocampal/amnesia patients 9. Fear conditioning a rat a. Freezing b. No reaction to both no freezing c. Damaging the direct and indirect pathway (since it leads to thalamus) no fear + fully deaf d. Yes they will freeze for both since only the indirect pathway is destroyed AKA loss of discrimination e. NO freezing because it cannot learn to fear it.
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