Hyperexcitability of pyramidal neurons in field CA1 in hippocampal slices from rats evoked by episodes of hypoxia: The roles of GABAA and GABAB receptors

摘要

Brain hypoxia/ischemia is known to be one of the leading causes of convulsive disorders in humans [4, 7]. The cellular mechanisms of posthypoxic hyperexcitability of brain neurons largely remain unstudied. In particular, the comparative roles of glutamate and GABA receptors in the development of this hyperexcitability remain unclear. Our previous studies demonstrated that periodic transient episodes of hypoxia induce stable epileptiform evoked discharges of population spikes in pyramidal neurons in field CA1 in hippocampal slices [1, 2, 6]. These discharges are accompanied by long-term potentiation of excitatory glutamatergic transmission in CA3–CA1 synapses and were dependent on the functional activity of both AMPA and NMDA glutamate receptors and L-type potential-dependent calcium channels.