METABOTROPIC GLUTAMATE-RECEPTOR DEPENDENT EPSP AND EPSP-SPIKE POTENTIATION IN AREA CA1 OF THE SUBMERGED RAT HIPPOCAMPAL SLICE

1. We reexamined the important areas of conflict in (1S,3R)-1-aminocyc lopentane-1,3-dicarboxylic acid [(1S,3R)-ACPD]-induced potentiation of the field excitatory postsynaptic potential (EPSP) and, for the first time, investigated the role of mGluRs in EPSP-spike (E-S) coupling. 2 . (1S,3R)-ACPD (10 mu M) bath applied for 20 min consistently induced a long-lasting potentiation of the dendritic EPSP in area CAI of subme rged rat hippocampal slices, which was considerably Easter in onset th an described previously. 3. This effect was not associated with any ch ange in presynaptic fiber volley but was dependent on both an intact C A3 connection, because removal of area CA3 blocked (1S,3R)-ACPD-induce d potentiation, and also on functional N-methyl-D-aspartate (NMDA) rec eptors, because (1S,3R)-ACPD-induced potentiation was blocked by inclu sion of the NMDA receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid (AP5; 50 mu M). 4. (1S,3R)-ACPD induced a long-lasting potentiat ion of the population spike (PS) amplitude that was consistently large r than that of the EPSP measured in the cell body area. This EPSP-PS ( E-S) potentiation was blocked by inclusion of the gamma-aminobuturic a cid-A (GABA(A)) receptor antagonist, picrotoxin (50 mu M). 5. E-S pote ntiation induced by high-frequency stimualtion (HFS), which was of the same magnitude as that induced by (1S,3R)-ACPD, was blocked by the mG luR-selective antagonist (+)-alpha-methyl-4-carboxyphenylglycine (+MCP G; 250 mu M). +MCPG also blocked HFS-induced long-term potentiation (L TP) of the EPSP measured in the cell body. 6. These results suggest th at (1S,3R)-ACPD-induced potentiation is NMDA receptor dependent, contr ary to some previous findings, and provide further evidence that both synaptic and E-S potentiation induced by (1S,3R)-ACPD share common mec hanisms of expression with HFS-induced LTP. The data emphasize the imp ortant role of mGluRs in induction of EPSP LTP and E-S potentiation.