Synapses in general exhibit various forms of plasticity; that is, the efficiency of transmission across the synapse can be potentiated or depressed in response to a prior history of stimulation. The persistence of the change in efficiency can be relatively brief, exemplified by post-tetanic potentiation (PTP), which decays within a few seconds. At the other extreme, very stable forms of plasticity, long-term potentiation (LTP) and long-term depression (LTD), can be established at many synapses in the brain. LTP is often proposed as a candidate for the cellular basis of memory, but direct evidence for this hypothesis is lacking. That said, a large body of research has provided correlative evidence for LTP as a process that underlies memory formation. This lecture, which is a part of the course "Cell Signaling Systems: A Course for Graduate Students," describes LTP from a cell biological perspective. Topics include the signaling network responsible for LTP induction, evidence for upregulated postsynaptic mechanisms in LTP, and the role of gene expression regulation, at the transcriptional and translational levels, in the maintenance of LTP.


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      NSDL,NSDL_SetSpec_BEN,signal transduction,synaptic plasticity,long-term potentiation,NMDA,memory,Life Science,oai:nsdl.org:2200/20080618224502014T,postsynaptic signaling



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