CSB332H1 Lecture Notes - Lecture 13: Synaptic Plasticity, Temporal Lobe, Episodic Memory

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coppercattle724

11 Aug 2012

School

UTSG

Department

Cell and Systems Biology

Course

CSB332H1

Professor

Melanie Woodin

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Document Summary

Synaptic modifications in cultured hippocampal neurons: dependence on. Spike timing, synaptic strength, and postsynaptic cell type. The journal of neuroscience, december 15, 1998, 18(24):10464- Instead of inducing ltp w high-freq presynaptic stimulation, spike- timing protocols use lower-freqs w paired pre- & postsynaptic activity (+)ve spike-timing interval: epsp arrives before postsynaptic ap is fired (-)ve spike-timing interval: epsp arrives after postsynaptic ap is fired. Pair pre & postsynaptic act pots during induction. Decide ahead of time what protocol to use, can choose from 2 intervals: Positive spike-timing intervals induce ltp: pair pre & post activity, regulate timing interval, uses dif ones. Negative spike timing intervals induce ltd (pair epsps w postsynaptic act pot: reverse order of pairing, post then pre, can get another act pot during repolarization phase. Post then pre, same timing, about 10ms interval. Critical window for induction of synaptic potentiation & depression.

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Botulinus toxin causes paralysis. It binds to presynaptic sitesat the motor end plate (neuromuscular junction) and prevents theexocytotic release of transmitter from vesicles. Predict theconsequences (increase, decrease, no change & explain why) ofblocking the release of acetylcholine at the neuromuscular junctionon the following: 1. Presynaptic resting potential 2. Presynapticaction potential amplitude 3. Presynaptic Ca2+ influx 4.Presynaptic transmitter release 5. Postsynaptic resting potential6. Postsynaptic end plate potential 7. Postsynaptic actionpotential amplitude 8. Postsynaptic action potential frequency 9.Muscle contractile strength

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Botulinus toxin causes paralysis. It binds to presynaptic sites at the motor end plate (neuromuscular junction) and prevents the exocytotic release of transmitter from vesicles. Predict the consequences (increase, decrease, no change & explain why) of blocking the release of acetylcholine at the neuromuscular junction on the following: 1. Presynaptic resting potential 2. Presynaptic action potential amplitude 3. Presynaptic Ca2+ influx 4. Presynaptic transmitter release 5. Postsynaptic resting potential 6. Postsynaptic end plate potential 7. Postsynaptic action potential amplitude 8. Postsynaptic action potential frequency 9. Muscle contractile strength

periwinklegoose111

Changes in the interaction between neurons or neural plasticityoccur throughout the nervous system. In particular, it is believedthat synaptic plasticity in the hippocampus is critical for storingspecific types of information that are involved in thepsychological process of memory. There is extensive evidenceindicating that specific glutamate receptors atasymmetric/excitatory synapses are involves in specific aspects ofacquisition and maintenance/expression of synaptic plasticity.

Describe the roles of the NMDA and AMPA receptors in synapticplasticity within in the hippocampus. Your answer should addressthe nature of the input necessary to induce synaptic plasticity andhow each of these receptors contribute to that process, including abrief description of downstream signaling. As well as, attributesof these receptors that allow them to perform specific roles insynaptic plasticity

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CSB332H1 Lecture Notes - Lecture 13: Synaptic Plasticity, Temporal Lobe, Episodic Memory

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