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Long‐lasting potentiation of synaptic transmission in the schaffer collateral‐commissural pathway of the guinea pig hippocampus by activation of postsynaptic N‐methyl‐D‐aspartate receptor
Author(s) -
Kamiya Haruyuki,
Sawada Satsuki,
Yamamoto Chosaburo
Publication year - 1993
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.890130210
Subject(s) - long term potentiation , schaffer collateral , post tetanic potentiation , postsynaptic potential , nmda receptor , excitatory postsynaptic potential , neurotransmission , neuroscience , biology , ltp induction , chemistry , inhibitory postsynaptic potential , receptor , biochemistry
Abstract The effects of short‐period (2 min) perfusion of conditioning solution, which contains N‐methyl‐D‐aspartate (NMDA), glycine, and spermine, on the synaptic transmission in the Schaffer collateral‐commissural pathway were examined in hippocampal slices with the intracellular recording technique. Long‐lasting potentiation of excitatory postsynaptic potentials (EPSPs) was induced (as long as the records lasted, up to 3 h in the longest observation) after membrane potentials of postsynaptic neurons were depolarized by current injection during perfusion of the conditioning solution. D‐2‐amino‐5‐phoshonovaleric acid (D‐AP5), a specific antagonist of NMDA receptors, block the induction of the long‐lasting potentiation by perfusion of NMDA containing solution. This potentiation was accompanied by a decrease in the relative magnitude of EPSP amplitude fluctuation (coefficient of varation, CV). The reciprocals of squared CVs (= mean 2 /variance) were almost proportional to the magnitude of the potentiation, and the ratios of 1/CV 2 and the magnitudes of potentiation were not different from those of long‐term potentiation (LTP) induced by tetanic stimulation. These findings suggest that long‐lasting potentiation is induced solely by activation of postsynaptic NMDA receptors, and transmitter release from presynaptic terminals may be modified by the activation of postsynaptic receptors. © 1993 Wiley‐Liss, Inc.