A bicuculline‐resistant inhibitory post‐synaptic potential in rat hippocampal pyramidal cells in vitro.

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Abstract
Experiments were performed on art hippocampal CA1 pyramidal cells in vitro to elucidate the origin of the late hyperpolarizing potential, which follows the GABA-mediated inhibitory post-synaptic potential (GABA-i.p.s.p.). The late hyperpolarizing potential could be evoked by orthodromic stimulation via stratum radiatum or stratum oriens but not by selective antidromic stimulation. The membrane soluble analog of cAMP, 8-Br cAMP, which blocks Ca-activated K hyperpolarizations (GK(Ca)), did not reduce the late hyperpolarizing potential. The enkephalin analog, (D-ala2-met5)-enkephalinamide (DALA) reversibly reduced both the GABA-i.p.s.p. and the late hyperpolarizing potential. The later hyperpolarizing potential and GABA-i.p.s.p. were more sensitive to low doses of the Ca antagonist, Cd, than the excitatory post-synaptic potential (e.p.s.p.). The local application of Cd to the pyramidal cell layer blocked the antidromic i.p.s.p. but the orthodromically evoked late hyperpolarizing potential was less affected. In contrast to the GABA-i.p.s.p., the late hyperpolarizing potential was not reversed by Cl injection and was enhanced, rather than depressed, by bicuculline. Evidently, the late hyperpolarizing potential is a bicuculline-resistant i.p.s.p. The unidentified transmitter for this i.p.s.p. is released from feed-forward interneurons primarily onto the dendrites of the pyramidal cell and may act by increasing the K permeability of the membrane. The epileptiform burst after-hyperpolarization evoked in the presence of GABA antagonists is composed of at least 2 components, a long-duration hyperpolarization mediated by GK(Ca) and an earlier and shorter late hyperpolarizing potential. Blockade of the GK(Ca) by 8-Br cAMP did not alter the duration of epileptiform bursts but did markedly increase the frequency of their occurrence. This suggests that GK(Ca) is involved in controlling the interval between bursts.