cell mechanism of learning/mem (7) Flashcards
in patient H.M. what part of his brain was removed and why?
hippocampus to get rid of seizures
what was the consequence of removing H.M.’s hippocampus?
inability to form new memories. tells you that new memories are made in the hippocampus
where is long term declarative memory stored?
a variety of cortical sites: wernicke’s area for the meaning of words, and the temporal cortex for the memories of objects & faces
where is long term non-declarative memory stored?
cerebellum, basal ganglia, pre motor cortex and other sites that are related to motor behavior
what does long term potentiation mean?
there is long lasting enhancement in signal transmission between two neurons that results from stimulating them synchronously.
synapses are able to change their strength!
what are the 3 pathways form the intrinsic trisynaptic circuitry?
- perforant path
- dentate granule cell projections to area CA3 pyrimidal cells
- CA3 pyramidal cell projections to CA1 pyrimidal cells
at low frequency & low intensity stimuli, which receptors are activated?
only the AMPA receptors
what are 2 NMDA receptor antagonists?
AP5 and MK801
is NMDA receptor activation required for LTP induction?
YES
for the NMDA receptor, what is the ion in its associated ion channel blocker?
Mg++
what would be the result on LTP if there was treatment with the protein synthesis inhibitor: aniosomycin?
LTP would decay within a few hours because protein synthesis is essential for LTP maintenance
what does PKA and CaMKII do to AMPA receptors?
it increases AMPA receptor currents by insertion of additional AMPA receptors
what two compounds increase NMDA currents?
PKC and PTK
what is the main way that the LTP pathway differs form the LTD pathway?
rises in Ca++ leads to the activation of phosphatases in the LTD pathway (where as in the LTP pathway it leads to activation of kinases)
what happens to the AMPA receptors in LTD?
they get internalized (which decreases the sensitivity to glutamate release)
