Learning and Memory 3: Cellular Basis Flashcards
Prof. Abel’s definition of learning vs. memory?
Learning: Experience-dependent behavioral changes
Memory: Retention of that behavioral change
3 different types of learning? Key area of brain?
Non-associative: Sensitization / habituation to a single stimulus (e.g. gill organ retraction) - reflexes?
Classical: Learning that one stimulus is often associated by another. (eg. Pavlov’s dog) - hippocampus
Operant/instrumental: Learning that a behavior results in a stimulus. (eg. press lever to get food) - striatum, dopanergic systems
What’s the name for the mechanism by which tail shock may sensitize the siphon-touch / gill-retraction reflex in Aplysia?
Presynaptic facilitation.
What’s the name for the process in which sensitization transitions to “memory”?
Long term potentiation (LTP): Synapses are facilitated even in the absence of pre-synaptic facilitation (eg. tail shock).
What is the molecular pathway used in pre-synaptic facilitation? (neurotransmitter, receptor, 2nd messengers, downstream effects, etc.)
tail-shock neuron makes serotonin –> cAMP –> PKA
PKA –> opens K+ channels to decrease AP threshold
PKA –> phosphorylates CREB –> gene transcription -> LTP
Outline the tri-synaptic circuit of the hippocampus. List the origin, cells, and named fibers connecting the cells.
Entorhinal cortex – (Perforant path) –> Granule cells in the dentate gyrus – (mossy fibers) –> CA3 pyramidal cells – (Schaffer collaterals) –> CA1 pyramidal cells
Say you have two neurons that both act pre-synaptically on another neuron. You give a tetanic stimulus to one but not the other. Will you see signs of early LTP (E-LTP) in both cells? What property does this illustrate?
No. You will only see signs of LTP from the neuron in which you produced a tetanic stimulus. This illustrates the concept of “Pathway Specificity” in LTP.
4 Properties of LTP?
Rapid onset
Long Lasting
Pathway Specificity
Associativity
How can the coincidence of post-synaptic and pre-synaptic depolarization be detected in the post-synaptic cell? What property of LTP does this illustrate?
Depolarization of presynaptic cell -> release of glutamate -> acts on AMPA -> Na+ influx -> post-synaptic depolarization
Post-synaptic cell depolarization -> NMDA activation -> Ca++ influx -> LTP-related changes (PKC, phosphorylation…)
Provides a possible mechanism for “associativity” in LTP.
What are the changes in the synapse that lead to E-LTP (early LTP) or E-LTD (long term depression, the opposite of LTP)?
Increased AMPA receptors on membrane -> E-LTP
Decreased AMPA receptors on membrane -> E-LTD
Main difference between E-LTP and L-LTP (late LTP)?
Early: modification of receptors at synapses.
Late: transcriptional change (PKA -> CREB, CRE et al.)
Two molecular targets you can inhibit to prevent LTP?
NMDA receptor (probably why ketamine can be used for date rape... no good) Calmodulin Kinase II (Cam kinase II) -mediates changes in E-LTP
