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We examined the effects of GABA receptor stimulation on the neuronal death induced by exogenously added excitatory amino acids or combined oxygen–glucose deprivation in mouse cortical cell cultures. Death induced by exposure to NMDA, AMPA, or kainate was attenuated by addition of GABA or the GABA A  receptor agonist, muscimol, but not by the GABA B  receptor agonist, baclofen. The antiexcitotoxic effect of GABA A  receptor agonists was blocked by bicuculline or Picrotoxin. In contrast, GABA or muscimol, but not baclofen, markedly increased the neuronal death induced by oxygen–glucose deprivation. Muscimol potentiation of neuronal death was associated with increased glutamate efflux to the bathing medium, and increased cellular  45 Ca 2+  accumulation; it was blocked by MK-801, but not NBQX, suggesting mediation by NMDA receptors. Bicuculline only weakly attenuated muscimol potentiation of oxygen–glucose deprivation-induced neuronal death, probably because it itself increased this death. Present results raise a note of caution in the proposed use of GABA A  receptor stimulation to limit ischemic brain damage in vivo.

GABAA Receptor Activation Attenuates Excitotoxicity but Exacerbates Oxygen—Glucose Deprivation-Induced Neuronal Injury In Vitro

GABA_A Receptor Activation Attenuates Excitotoxicity but Exacerbates Oxygen—Glucose Deprivation-Induced Neuronal Injury In Vitro