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Urs 5357 Neurobiology Exam 2 Test Bank Complete Questions And Answers Already Passed Resource

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URS 5357 NEUROBIOLOGY EXAM 2 TEST BANK COMPLETE QUESTIONS AND ANSWERS ALREADY PASSED RESOURCE

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NURS 5357 NEUROBIOLOGY EXAM 2 TEST
BANK COMPLETE QUESTIONS AND
ANSWERS ALREADY PASSED RESOURCE

●● what is anti-hebbian plasticity?
Answer: - a learning rule by which synaptic plasticity can be controlled
- reduction in strength of synaptic connectivity between neurons


●● what was hebb's rule?
Answer: neurons that fire together, wire together


●● what is the best studied form of synaptic weakening?
Answer: cerebellar long term depression


●● what is the functional debate among cerebellar LTD?
Answer: - fine tuner of movement
- motor learning
- error adjustment
- higher cognitive processes


●● the cerebellar circuitry of LTD is a form of what important neuron
factor?

,Answer: convergence


●● what are the three factors in cerebellar circuitry?
Answer: - granule cells
- purkinje cells
- climbing fiber


●● how does cerebellar circuitry work?
Answer: Purkinje cells receive excitatory input from granule cells and
climbing fibers:
a) parallel fibers of granule cells have weak synapses, release glutamate
resulting in weak depolarization of purkinje cell
- purkinje cell can fire only if all parellel fibers are activated at once
b) climbing fiber fires AP, releasing glutamate resulting in a strong
depolarization of purkinje cell
- purkinje cell almost always fires AP in response


●● where does the climbing fiber come from and what does it do?
Answer: medulla; wraps around dendrites of purkinje cell


●● what is important about the input to granule cells?
Answer: they are spatially summated

,●● what happens when parallel fibers and climbing fibers are constantly
fired together?
Answer: - parallel fiber input decreases in strength (demonstrating LTD
and anti-hebbian plasticity)


●● Walk through the simultaneous firing of climbing fibers and parallel
fibers in cerebellar LTD.
Answer: 1. postsynaptic depolarization from climbing fiber activation
causes glutamate to bind to NMDA
- opens NMDA causing Ca2+ influx into intracellular space at CF
synapse
2. At the same time, glutamate binds to metabotropic receptors in PF/PC
synapse
- g-protein activates enzyme phospholipase C
- phospholipase C produces inositol triphosphate (IP3) in cytosol
- IP3 binds to IP3 gated calcium channels on endoplasmic reticulum,
causing efflux of Ca2+ into intracellular space
3. Sharp rise of calcium from both synapses triggers activation of protein
kinase C (PKC)
4. PKC phosphorylates AMPA receptors, promoting dissociation and
internalization AT PF/PC synapse (removal)
5. With AMPA receptors lost, postsynaptic response in purkinje cell from
glutamate in parallel cells is depressed


*level of calcium needed for PKC is not attainable by only one synapse

, ●● what does phosphorylate mean?
Answer: change in protein behavior


●● cerebellar LTD is a form of what homeostatic mechanism?
Answer: positive feedback loop


●● what is a device that translates neuronal information into commands
capable of controlling external software/hardware?
Answer: brain machine interface (BMI)


●● why would BMI be used?
Answer: used for people who have sensory or motor impairment (ie
paralysis)


●● how does BMI work?
Answer: - targets motor cortex
- records activity of multiple neurons as organism performed diverse
motor movements
- computer identifies correlations between patterns of movement =
patterns of neuron activity


●● what does a decoder do in BMI?

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