LONG-TERM POTENTIATION INDUCED BY SINGLE VOLLEY ACTIVATION - A MECHANISM FOR BICUCULLINE-INDUCED ENHANCEMENT OF SYNAPTIC FIELD POTENTIALS IN THE CA1 HIPPOCAMPAL REGION

Long-term potentiation in the CA1 region is often evaluated as the cha nge in the initial slope of the field response following a single test stimulus. This change is thought to represent an alteration of excita tory transmission only. However, it has recently been reported that th is initial part of the field response is also controlled by a picrolox in-resistant GABA(A)ergic response since bicuculline (100 mu M), in th e presence of picrotoxin, could lead to a substantial increase in the field response initial slope. A disinhibition may then be an important factor underlying expression of what is believed to be long-term pote ntiation of excitatory synaptic transmission. Alternatively, the bicuc ulline-induced field response enhancement could be due to an induction of long-term potentiation favoured by the low magnesium (1.25 mM) and high calcium (4 mM) concentrations used in these experiments. Results presented here show that neither picrotoxin (100 mu M), nor bicuculli ne (100 mu M), produce any significant change in field response initia l slope, when examined using 4 mM magnesium and calcium in the perfusi on fluid. In experiments using lower magnesium (1-1.5 mM), the same re sult was observed in most cases. In some cases, the field response fol lowing single test stimuli became temporally paired with spontaneous b ursts of spike activity, and its initial slope became considerably enh anced (100%). Similar results could be provoked by a temporary increas e in stimulus strength sufficient to evoke spike activity. This potent iation occluded a subsequent long-term potentiation induced by afferen t tetanization, and it was not observed when a N-methyl-D-aspartate re ceptor antagonist was present in the perfusion solution. The present r esults suggest that the bicuculline induced enhancement of the field r esponse initial slope represents an induction of long-term potentiatio n rather than being a direct consequence of pharmacological blockade o f a GABA(A)ergic process. (C) 1997 IBRO.