Histamine and noradrenaline decrease calcium-activated potassium conductance in hippocampal pyramidal cells.
Ample evidence exists for histaminergic and noradrenergic projections to the hippocampus. Both amines exert neurotransmitter or modulator actions on principal neurones in the CA 1 and in the dentate area. A number of mechanisms have been proposed for these actions, including increased potassium conductance, increased chloride conductance and electrogenic pump stimulation, and reduction of the anomalous inward rectification. Action potentials, and particularly bursts of spikes, in CA 1 pyramidal cells, are followed by an afterhyperpolarization (AHP) which consists of two components. The late AHP depends on a calcium-activated potassium conductance gK+ (Ca2+), and has recently been shown to be increased by dopamine. We report here a rapid and reversible decrease of the late AHP component following a burst of sodium spikes or a calcium spike, during perfusion with micromolar concentrations of histamine and noradrenaline. This effect is mediated by H2 receptors and beta-receptors, respectively, and occurred in the absence of changes in the calcium spike. By such a mechanism histamine and noradrenaline can profoundly potentiate the excitatory impact of depolarizing signals.
D000818:Animals; D002118:Calcium / Q000502:physiology*; D004298:Dopamine / Q000494:pharmacology; D006624:Hippocampus / Q000502:physiology*; D006632:Histamine / Q000502:physiology*; D007473:Ion Channels / Q000502:physiology; D007545:Isoproterenol / Q000494:pharmacology; D008564:Membrane Potentials / Q000187:drug effects; D009638:Norepinephrine / Q000502:physiology*; D011188:Potassium / Q000502:physiology*; D051381:Rats; D011943:Receptors, Adrenergic, beta / Q000502:physiology; D011970:Receptors, Histamine H2 / Q000502:physiology
D007473:Ion Channels; D011943:Receptors, Adrenergic, beta; D011970:Receptors, Histamine H2; D006632:Histamine; D007545:Isoproterenol; D011188:Potassium; D002118:Calcium; D004298:Dopamine; D009638:Norepinephrine