Jhamandas J H, Renaud L P
Am J Physiol. 1987 May;252(5 Pt 2):R947-52. doi: 10.1152/ajpregu.1987.252.5.R947.
The excitability of vasopressin-secreting neurons in the hypothalamic supraoptic nucleus is transiently depressed by an abrupt increase in arterial pressure sufficient to activate peripheral arterial baroreceptors. The present experiments examined the ability of locally applied transmitter antagonists to alter this response. Extracellular data were obtained from 27 supraoptic vasopressin-secreting neurons in pentobarbital-anesthetized male Long-Evans rats. In seven of eight cells tested, bicuculline (100 microM) reversibly abolished or delayed the anticipated cessation in neuronal firing that accompanied a 40- to 60-mmHg increase in arterial pressure induced by a brief intravenous infusion of the alpha-agonist metaraminol. Similar tests applied to the remaining cells revealed that prazosin (10 microM), timolol (20 microM), or strychnine (100 microM) were ineffective. These findings suggest that gamma-aminobutyric acidA receptors mediate the depressant responses observed among supraoptic vasopressin-secreting neurons consequent to peripheral baroreceptor activation.
足以激活外周动脉压力感受器的动脉压突然升高会使下丘脑视上核中分泌血管加压素的神经元的兴奋性短暂降低。本实验研究了局部应用递质拮抗剂改变这种反应的能力。从戊巴比妥麻醉的雄性Long-Evans大鼠的27个视上核分泌血管加压素的神经元中获取细胞外数据。在测试的8个细胞中的7个中,荷包牡丹碱(100微摩尔)可逆地消除或延迟了神经元放电预期的停止,这种停止伴随着通过短暂静脉注射α-激动剂间羟胺诱导的动脉压升高40至60毫米汞柱。对其余细胞进行的类似测试表明,哌唑嗪(10微摩尔)、噻吗洛尔(20微摩尔)或士的宁(100微摩尔)无效。这些发现表明,γ-氨基丁酸A受体介导了在视上核分泌血管加压素的神经元中因外周压力感受器激活而观察到的抑制反应。