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Postsynaptic modulation of NMDA synaptic currents in rat hippocampal microcultures by paired‐pulse stimulation.
Author(s) -
Mennerick S,
Zorumski C F
Publication year - 1996
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1996.sp021154
Subject(s) - ampa receptor , nmda receptor , long term depression , excitatory postsynaptic potential , neuroscience , postsynaptic potential , postsynaptic current , glutamate receptor , chemistry , biology , inhibitory postsynaptic potential , receptor , biochemistry
1. Paired‐pulse synaptic stimulation of hippocampal neurons in microcultures resulted in depression of synaptic currents mediated by both NMDA and alpha‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionate (AMPA) receptors. However, NMDA EPSCs were more severely depressed than AMPA EPSCs. 2. Partial NMDA receptor blockade reduced paired‐pulse depression of NMDA but not of AMPA synaptic currents while partial AMPA receptor blockade had no effect on paired‐pulse depression of AMPA EPSCs. These results suggest that ion flux through NMDA receptors is important in paired‐pulse depression of NMDA responses but has no effect on AMPA responses. 3. Low extracellular Ca2+ concentrations or positive postsynaptic holding potentials reduced paired‐pulse depression of NMDA EPSCs to near that of AMPA responses. 4. Brief paired applications of exogenous glutamate to neurons produced Ca(2+)‐dependent depression similar to the depression of NMDA synaptic responses and synaptic stimulation depressed responses to exogenously applied NMDA. 5. Physiological concentrations of Mg2+ prevented expression of the postsynaptic modulation of NMDA EPSCs at ‐70 mV, but partial relief of Mg2+ block of the NMDA channel with depolarization increased paired‐pulse depression of NMDA EPSCs.