TRANSIENT ISCHEMIA INDUCES AN EARLY DECREASE OF SYNAPTIC TRANSMISSIONIN CA1 NEURONS OF RAT HIPPOCAMPUS - ELECTROPHYSIOLOGIC STUDY IN BRAIN-SLICES

We examined the functionality of hippocampal CA1 neurons at early time s after transient global ischemia, by electrophysiologic recordings in brain slices. Transient ischemia was conducted on rats using the meth od of 15-minute four-vessel occlusion, and brain slices were obtained from these animals at different times after ischemia. Within 24 hours after insult, CA1 neurons showed no substantial damage as identified b y morphologic means, but exhibited dramatic decreases in synaptic acti vities by 12 hours after insult, which became further decreased at mor e extended times after recovery. Blocking gamma-aminobutyric acid A (G ABA(A)) receptors with bicuculline produced a reversible augmentation of the diminished synaptic responses in slices prepared from 12-hour p ostinsult animals, but failed to do so in slices obtained from rats 24 hours after insult. Recorded in whole-cell mode, the minimum depolari zing current required to elicit an action potential was about twofold larger in the ischemic CA1 neurons than in sham controls, suggesting t hat an elevated spiking threshold exists in these neurons. We suggest that decreases in electrophysiologic activities precede the morphologi c deterioration in postischemic CA1 neurons. The early decrease in CA1 synaptic activities may be associated with an imbalance between gluta mate-mediated synaptic excitation and GABA(A)-mediated synaptic inhibi tion, whereas substantial impairments in synaptic transmission likely take place after prolonged post ischemic recovery.