Histamine potentiates neuronal excitation by blocking a calcium-dependent potassium conductance.
Histaminergic neurones send their axons to the whole forebrain. The diffuse projection is consistent with a modulatory role of these pathways. In hippocampal slices from rats a mechanism for this modulation is described, on pyramidal neurones of the CA 1 area: Strong excitations induced by intracellular current injection, ionophoretic administration of glutamate or synaptic stimulation normally restrict themselves by the activation of the calcium-dependent potassium current (gK(Ca) ). This current causes a long lasting afterhyperpolarization and an accommodation of firing. Their block by histamine and impromidine (reversed by metiamide and cimetidine) leads to a profound potentiation of excitatory signals. It is suggested that HA, through H2 receptors, accelerates the removal of intracellular free Ca++ ions.
D000818:Animals; D002118:Calcium / Q000502:physiology*; D006632:Histamine / Q000494:pharmacology*; D007093:Imidazoles / Q000494:pharmacology; D017446:Impromidine; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D009431:Neural Conduction / Q000187:drug effects*; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D011188:Potassium / Q000502:physiology*; D051381:Rats; D009435:Synaptic Transmission / Q000187:drug effects
D007093:Imidazoles; D006632:Histamine; D017446:Impromidine; D011188:Potassium; D002118:Calcium