The ionic dependence of the histamine-induced depolarization of vasopressin neurones in the rat supraoptic nucleus.
1. The ionic basis of the histamine-induced depolarization of immunohistochemically identified neurones in the supraoptic nucleus (SON) was investigated in the hypothalamo-neurohypophysial explant of male rats. Histamine (0.1-100 microM) caused an H1 receptor-mediated, dose-dependent depolarization of fifty of sixty-two vasopressin neurones in the SON. In contrast, twenty-three oxytocin neurones were either depolarized (n = 6), hyperpolarized (n = 4), or unaffected (n = 13) by histamine. Due to the low percentage of responding cells, oxytocin neurones were not further investigated. 2. Chelation of intracellular Ca2+ with 1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid (BAPTA; 100-500 mM) blocked the depolarization, whereas blocking Ca2+ influx and synaptic transmission with equimolar Co2+ or elevated (5-20 mM) Mg2+ in nominally Ca(2+)-free solutions was without effect. 3. The amplitude of the histamine-induced depolarization was relatively independent of membrane potential. The input resistance was unaltered by histamine in nine neurones, but in nine other neurones it was decreased and in two neurones it was increased by more than 5%. Neither elevating extracellular K+ nor addition of the K+ channel blockers, apamin, d-tubocurarine, tetraethylammonium (TEA), or intracellular Cs+ decreased the histamine effect. Indeed, broadly blocking K+ currents with TEA and Cs+ significantly increased the depolarization to histamine. 4. Tetrodotoxin (2-3 microM) did not inhibit the histamine-induced depolarization. However, equimolar replacement of approximately 50% of extracellular Na+ with Tris+ or N-methyl-D-glucamine reduced or eliminated the response. 5. The depolarization of vasopressin neurones by histamine thus requires extracellular Na+ and intracellular Ca2+. Activation of a Ca(2+)-activated non-specific cation current or a Ca(2+)-Na+ pump are possible mechanisms for this effect.
Department of Anatomy and Neurobiology, Colorado State University, Fort Collins 80523, USA.
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Smith
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Armstrong
D000818:Animals; D001710:Biotin; D002118:Calcium / Q000502:physiology; D002614:Chelating Agents / Q000494:pharmacology; D004594:Electrophysiology; D006632:Histamine / Q000494:pharmacology*; D017442:Histamine Agonists / Q000494:pharmacology; D006633:Histamine Antagonists / Q000494:pharmacology; D007030:Hypothalamo-Hypophyseal System / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D007150:Immunohistochemistry; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D018408:Patch-Clamp Techniques; D010913:Pituitary-Adrenal System / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013495:Supraoptic Nucleus / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D013569:Synapses / Q000187:drug effects / Q000502:physiology; D014667:Vasopressins / Q000502:physiology*
D002614:Chelating Agents; D017442:Histamine Agonists; D006633:Histamine Antagonists; D014667:Vasopressins; D001710:Biotin; D006632:Histamine; D002118:Calcium