THE IONIC DEPENDENCE OF THE HISTAMINE-INDUCED DEPOLARIZATION OF VASOPRESSIN NEURONS IN THE RAT SUPRAOPTIC NUCLEUS

1. The ionic basis of the histamine-induced depolarization of immunohi stochemically identified neurones in the supraoptic nucleus (SON) was investigated in the hypothalamo-neurohypophysial explant of male rats. Histamine (0.1-100 mu M) caused an H-1 receptor-mediated, dose-depend ent depolarization of fifty of sixty-two vasopressin neurones in the S ON. In contrast, twenty-three oxytocin neurones were either depolarize d (n = 6), hyperpolarized (n = 4), or unaffected (n = 13) by histamine . Due to the low percentage of responding cells, oxytocin neurones wer e not further investigated. 2. Chelation of intracellular Ca2+ with ,2 -bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA; 100-500 mM) blocked the depolarization, whereas blocking Ca2+ influx and synap tic transmission with equimolar Co2+ Or elevated (5-20 mM) Mg2+ in nom inally Ca2+-free solutions was without effect. 3. The amplitude of the histamine-induced depolarization was relatively independent of membra ne potential. The input resistance was unaltered by histamine in nine neurones, but in nine other neurones it was decreased and in two neuro nes it was increased by more than 5%. Neither elevating extracellular K+ nor addition of the K+ channel blockers, apamin, d-tubocurarine, te traethylammonium (TEA), or intracellular Cs+ decreased the histamine e ffect. Indeed, broadly blocking K+ currents with TEA and Cs+ significa ntly increased the depolarization to histamine. 4. Tetrodotoxin (2-3 m u M) did not inhibit the histamine-induced depolarization. However, eq uimolar replacement of similar to 50% of extracellular Na+ with Tris() or N-methyl-D-glucamine reduced or eliminated the response. 5. The d epolarization of vasopressin neurones by histamine thus requires extra cellular Na+ and intracellular Ca2+. Activation of a Ca2+-activated no n-specific cation current or a Ca2+-Na+ pump are possible mechanisms f or this effect.