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Acute stress impairs (or induces) synaptic long‐term potentiation (LTP) but does not affect paired‐pulse facilitation in the stratum radiatum of rat hippocampus
Author(s) -
Shors Tracey J.,
Thompson Richard F.
Publication year - 1992
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/syn.890110311
Subject(s) - long term potentiation , excitatory postsynaptic potential , neural facilitation , neuroscience , postsynaptic potential , facilitation , ampa receptor , glutamate receptor , hippocampus , stimulation , neurotransmitter , ltp induction , biology , hippocampal formation , chemistry , medicine , inhibitory postsynaptic potential , receptor , central nervous system
Rats were exposed to restraint coupled with 60, 1‐sec, 1‐mA, 60‐Hz tail shocks. One hippocampus was immediately dissected for in vitro measurement of pairedpulse facilitation and LTP of the excitatory postsynaptic potential (EPSP) recording from the stratum radiatum of field CA1. There was no change in paired‐pulse facilitation, suggesting that acute exposure to the stressor does not result in a decrease in presynaptic neurotransmitter release. There was, however, a significant decrease in the percent LTP produced by theta burst stimulation relative to naïve controls. These results are consistent with the hypothesis that the stress‐induced impairment of LTP is a result of changes in the postsynaptic glutamate receptors, specifically the AMPA type. © Wiley‐Liss, Inc.