The ionic dependence of the histamine-induced depolarization of vasopressin neurones in the rat supraoptic nucleus

Bret N. Smith, William Armstrong

Research output: Contribution to journalArticle

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Abstract

1. The ionic basis of the histamine-induced depolarization of immunohistochemically identified neurones in the supraoptic nucleus (SON) was investigated in the hypothalamoneurohypophysial explant of male rats. Histamine (0.1-100 μM) 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 Ca2+-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 estracellular 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 μM) did not inhibit the histamine-induced depolarization. However, equimolar replacement of ~ 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 Ca2+-activated non-specific cation current or a Ca2+-Na+ pump are possible mechanisms for this effect.

Original languageEnglish (US)
Pages (from-to)465-478
Number of pages14
JournalJournal of Physiology
Volume495
Issue number2
DOIs
StatePublished - Sep 1 1996

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Supraoptic Nucleus
Vasopressins
Histamine
Neurons
Tetraethylammonium
Oxytocin
Histamine Agents
Apamin
Tubocurarine
Histamine H1 Receptors
Tetrodotoxin
Synaptic Transmission
Membrane Potentials
Cations

All Science Journal Classification (ASJC) codes

  • Physiology

Cite this

The ionic dependence of the histamine-induced depolarization of vasopressin neurones in the rat supraoptic nucleus. / Smith, Bret N.; Armstrong, William.

In: Journal of Physiology, Vol. 495, No. 2, 01.09.1996, p. 465-478.

Research output: Contribution to journalArticle

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abstract = "1. The ionic basis of the histamine-induced depolarization of immunohistochemically identified neurones in the supraoptic nucleus (SON) was investigated in the hypothalamoneurohypophysial explant of male rats. Histamine (0.1-100 μM) 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 Ca2+-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 estracellular 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 μM) did not inhibit the histamine-induced depolarization. However, equimolar replacement of ~ 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 Ca2+-activated non-specific cation current or a Ca2+-Na+ pump are possible mechanisms for this effect.",
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