ANOXIA BLOCKS THE PRESYNAPTIC CONTROL OF GABA RELEASE AT INHIBITORY TERMINALS IN THE RAT HIPPOCAMPUS

Field potential and (K+)(o) recordings were made in rat hippocampal sl ices during application of 4-aminopyridine (50 mu M) and ionotropic ex citatory amino acid receptor antagonists, to establish whether anoxia modifies the mechanisms that regulate GABA release from inhibitory int erneurons. Synchronous, negative-going field potentials (amplitude=1.4 1+/-0.64 mV, mean+/-S.D.; interval=40.9+/-15.7 s; n=10) occurred spont aneously in the CA3 stratum radiatum under control conditions. These e vents were associated with transient elevations in (K+)(o) (peak value s= 5.3+/-0.7 mM; duration=23.4+/-3.5 s; n=5 slices) and were abolished by the GABA(A) receptor antagonist bicuculline methiodide (10 mu M; n =5), the GABA(B) receptor agonist baclofen (100 mu M; n=6) or the mu-o pioid receptor agonist (D-Ala(2)-N-Me-Phe,Gly-ol) enkephalin (10 mu M; n=4). Hence they represented monosynaptic field inhibitory postsynapt ic potentials. Brief (4-5 min) episodes of anoxia induced a reversible , slow elevation of the baseline (K+)(o) to 5.2+/-0.3 mM (n=5), while the rate of the field inhibitory postsynaptic potentials increased by an average of 130.7% (n=10). Oxygen interruption during application of either baclofen (n=6) or (D-Ala(2)-N-Me-Phe,Gly-ol)enkephalin (n=4) b locked the depressant action of both drugs on the field inhibitory pos tsynaptic potential. These findings demonstrate that hippocampal monos ynaptic field inhibitory postsynaptic potentials are resistant to brie f anoxic episodes and that oxygen deprivation readily blocks the presy naptic control of GABA release exerted by GABA(B) and mu-opioid recept ors at inhibitory interneuron terminals. Copyright (C) 1996 IBRO. Publ ished by Elsevier Science Ltd.