1) What are the caveats of making the claim that LTP is a model for learning?

2) What is the connection between development of the nervous system and LTP/LTD as it is studied in hippocampal slices?

3) Why were the existence of retrograde messengers proposed to be critical for the induction of LTP? What are some of the molecules that are proposed to function as retrograde messengers .What common properties do these molecules have that allow them to function as retrograde messengers?

4) Use an example to discuss how associative LTD can be induced and what relevance this has to learning? What does it mean that this phenomenon is not very robust?

5) Since we already covered synaptic plasticity in the red nucleus corticorubral pathway, cerebellum parallel fibers - Purkinje cells, and Aplysia sensory - motor neuron why revisit this phenomenon with respect to the neocortex?

6) Draw the extracellular and intracellular response that you would see under the following conditions: At t=0 an action potential is generated in axon X. At t=1 GABA is released from axon X and AMPA receptor mediated channels start opening in the postsynaptic cell. The extracellular response is recorded at the point where the dot is located (left side of soma). Draw the responses on the  lines A (extracellular response) and B (intracellular response). No action potentials are generated in the postsynaptic cell.

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OAMG/AMB 1997