HYPOXIC BLOCKADE OF SYNAPTIC TRANSMISSION IN HIPPOCAMPUS

To understand how anoxia so rapidly interrupts brain function, electro physiological techniques have been used to analyze the effects of brie f anoxia, mainly on hippocampal pyramidal neurons in brain slices. A p rominent hyperpolarization and loss of excitability, generated by incr eased membrane potassium (K) conductance, probably accounts for the ea rly suppression of electrical activity. Evidence is given that the hei ghtened K conductance is caused by a rise in free cytosolic Ca2+, much of it released from a dantrolene sensitive internal store. Judging by the nonlinear voltage-dependence and susceptibility to block by carba chol, the K-channels involved may be of the M-type. An early transient depolarizing effect of anoxia is caused by a sustained inward current (possibly chloride-mediated), normally largely masked by the outward K current. Finally, anoxia has two other early effects: it reversibly suppresses Ca-currents, especially of the high-threshold variety, and selectively inactivates inhibitory synaptic potentials, owing to a pre synaptic block of inhibitory transmitter release.