Mechanisms underlying anoxic hyperpolarization of hippocampal neurons.

The outward current evoked in CA1 neurons by brief anoxia is strongly voltage dependent and is abolished by an atropine-sensitive action of carbachol (and also when recording with a GTP gamma S-containing microelectrode). In this respect, it closely resembles the M-type K current, but the involvement of other, voltage-independent, carbachol-sensitive K channels has not been excluded. When the anoxic outward current is eliminated, an anoxic inward current is revealed, which may be Cl- mediated. It is suggested that an early release of Ca2+ from a dantrolene (and perhaps GTP)-sensitive internal store activates Ca-sensitive Cl channels, as well as carbachol-sensitive (mainly M-type?) K channels. The opposing Cl- and K currents would account for the variable depolarizing and hyperpolarizing effects of anoxia.