Escape from inhibition of synaptic transmission during in vitro hypoxia and hypoglycemia in the hippocampus.

Electrophysiological recordings were made from rat hippocampal slices exposed to in vitro ischemic conditions in which the superfused medium is hypoxic and lacking glucose. Under these conditions, the evoked population spike recorded in CA1 is initially depressed and then transiently returns prior to an anoxic depolarization. This transient return in synaptic function under ischemic-like conditions also occurs if the population spike is inhibited by pretreatment with adenosinergic agonists or with the gamma-aminobutyric acid (GABA)B agonist, baclofen.