부산대학교 도서관

On rat hippocampal slices using a standard patch-clamp technique in the whole-cell configuration, we studied the effects of long-term (40 to 60 min) hypoxia/hypoglycemia (HH) on excitatory postsynaptic currents (EPSC) evoked by stimulation of Schaffer collaterals in the cells of the CA1 zone. In addition to the earlier described effect of an immediate drop in the EPSC amplitude, a significant transient increase in its amplitude 30–50 min after the beginning of HH was observed. A pharmacologically isolated NMDA component of excitatory synaptic events underwent similar changes: 30–50 min after the blockade of NMDA receptor-mediated current, a fast recovery of its amplitude to the control (or even higher) values occurred. A blocker of NMDA/glutamate (Glu) receptors, D-aminophosphonovaleric acid (D-APV), and a competitive nonspecific antagonist of metabotropic Glu receptors, (RS)-α-methyl-4-carboxyphenylglycine - (RS)-MCPG - did not influence the HH-induced initial suppression of synaptic transmission but completely eliminated its delayed recovery. Our findings allow us to suppose that NMDA receptors, as well as metabotropic Glu receptors, play important roles in the cascade of biochemical reactions resulting in death of hippocampal pyramidal cells in the course of and after long-term ischemia in vivo.