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全身性可乐定后视上核加压素神经元的抑制作用

Inhibition of supraoptic vasopressin neurones following systemic clonidine.

作者信息

Bailey A R, Clarke G, Wakerley J B

机构信息

Department of Anatomy, School of Medical Sciences, University of Bristol, UK.

出版信息

Neuropharmacology. 1994 Feb;33(2):211-4. doi: 10.1016/0028-3908(94)90010-8.

Abstract

Experiments were undertaken in urethane-anaesthetized rats to investigate the effects of systemic clonidine on the firing of supraoptic vasopressin (VP) neurones, which were identified by their characteristic phasic activity pattern. Injection of clonidine (50 micrograms/kg i.v.) reduced the firing of all 16 VP neurones tested, and their overall mean activity decreased from 5.09 +/- 1.01 to 1.63 +/- 0.64 spikes/second (P < 0.02). In VP cells which were already firing phasically before clonidine, the inhibition resulted in complete quiescence. In VP cells which were originally continuously active, the inhibition resulted in a switch to phasic activity. This inhibitory effect, which was prevented by prior injection of the alpha-2 antagonist idazoxan (0.5 mg/kg), had a mean duration of 11.8 +/- 1.8 min. Subsequent experiments revealed that i.v. clonidine (50 micrograms/kg) caused a transient rise in blood pressure, but this had a shorter time-course and was unlikely to account for the prolonged neuronal inhibition. It was concluded that systemic clonidine acts centrally to suppress the activity of hypothalamic VP neurones, thereby explaining the fall in plasma VP levels found in previous studies.

摘要

在乌拉坦麻醉的大鼠身上进行了实验,以研究全身性可乐定对视上核加压素(VP)神经元放电的影响,这些神经元通过其特征性的相位活动模式来识别。静脉注射可乐定(50微克/千克)可降低所测试的所有16个VP神经元的放电,其总体平均活动从5.09±1.01降至1.63±0.64个脉冲/秒(P<0.02)。在可乐定注射前已经进行相位放电的VP细胞中,抑制作用导致完全静止。在原本持续活跃的VP细胞中,抑制作用导致转变为相位活动。这种抑制作用可被预先注射α-2拮抗剂咪唑克生(0.5毫克/千克)所阻断,其平均持续时间为11.8±1.8分钟。随后的实验表明,静脉注射可乐定(50微克/千克)会导致血压短暂升高,但这种升高的时间过程较短,不太可能解释神经元的长期抑制。得出的结论是,全身性可乐定通过中枢作用抑制下丘脑VP神经元的活动,从而解释了先前研究中发现的血浆VP水平下降的原因。

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