Smith B N, Armstrong W E
Department of Anatomy and Neurobiology, College of Medicine, University of Tennessee, Memphis 38163.
Neuroscience. 1993 Apr;53(3):855-64. doi: 10.1016/0306-4522(93)90630-x.
Previous studies have demonstrated that histamine primarily excites unidentified neurons in the rat supraoptic nucleus. We investigated the neuromodulatory effects of histamine on immunohistochemically identified vasopressin neurons in the rat supraoptic nucleus using intracellular recording techniques from the hypothalamo-neurohypophysial explant. Exogenous application of histamine (0.1-100 microM) to vasopressinergic neurons produced a small membrane depolarization accompanied by an increase of up to 100% in the amplitude of the depolarizing afterpotential that follows current-evoked trains of action potentials. The enhancement of the depolarizing afterpotential by histamine did not depend upon the depolarization. Further, histamine enhanced the amplitude of the depolarizing afterpotential when blocking the afterhyperpolarizing potential with d-tubocurarine or apamin, and in the presence of tetrodotoxin and d-tubocurarine or apamin, indicating a postsynaptic action of histamine on the depolarizing afterpotential that is not simply a reflection of a decrease in the afterhyperpolarizing potential. These toxins also had no effect on the histamine-induced depolarization. The enhancement of the depolarizing afterpotential by histamine was mimicked by the histamine H1-receptor agonist 2-thiazolylethylamine and was reduced or blocked by the H1-receptor antagonist promethazine, but was not blocked or reduced in the presence of the histamine H2-receptor antagonist, cimetidine. In summary, these results show that the excitatory effect of histamine on immunohistochemically identified vasopressin neurons in the supraoptic nucleus is due in part to the H1-receptor-mediated enhancement of the depolarizing afterpotential independent of any change in the afterhyperpolarizing potential or membrane potential.
以往的研究表明，组胺主要兴奋大鼠视上核中未明确的神经元。我们使用下丘脑 - 神经垂体离体组织的细胞内记录技术，研究了组胺对大鼠视上核中免疫组化鉴定的加压素神经元的神经调节作用。向加压素能神经元外源性施加组胺（0.1 - 100微摩尔）会引起轻微的膜去极化，并伴随在电流诱发的动作电位串之后的去极化后电位幅度增加高达100%。组胺对去极化后电位的增强并不依赖于去极化。此外，当用筒箭毒碱或阿帕明阻断超极化后电位时，以及在存在河豚毒素和筒箭毒碱或阿帕明的情况下，组胺增强了去极化后电位，这表明组胺对去极化后电位的作用是突触后作用，并非仅仅是超极化后电位降低的反映。这些毒素对组胺诱导的去极化也没有影响。组胺对去极化后电位的增强作用被组胺H1受体激动剂2 - 噻唑基乙胺模拟，并被H1受体拮抗剂异丙嗪降低或阻断，但在组胺H2受体拮抗剂西咪替丁存在时并未被阻断或降低。总之，这些结果表明，组胺对视上核中免疫组化鉴定的加压素神经元的兴奋作用部分归因于H1受体介导的去极化后电位增强，与超极化后电位或膜电位的任何变化无关。
