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大鼠中对向中缝背核输注促甲状腺激素释放激素的升压和交感反应。

Pressor and sympathetic responses to dorsal raphe nucleus infusions of TRH in rats.

作者信息

Mattila J, Buñag R D

机构信息

Department of Pharmacology, College of Health Sciences and Hospital, University of Kansas Medical Center, Kansas City 66103.

出版信息

Am J Physiol. 1990 Jun;258(6 Pt 2):R1464-71. doi: 10.1152/ajpregu.1990.258.6.R1464.

Abstract

Pressor, tachycardic, and sympathoexcitatory responses to intracerebroventricularly (icv) infused thyrotropin-releasing hormone (TRH) were recorded in urethan-anesthetized rats to identify where centrally administered TRH acts in the brain. None of these responses was altered either by electrolytic lesions in the medial preoptic, posterior, or paraventricular hypothalamus or by chemical lesions produced by destroying catecholaminergic neurons with icv infused 6-hydroxydopamine. By contrast, when serotonergic neurons were similarly destroyed with 5,7-dihydroxytryptamine, TRH-induced tachycardia was inhibited. Attendant pressor responses were also inhibited by electrolytic lesions of the dorsal, but not of the median, raphe nucleus. Pressor and sympathoexcitatory responses elicited by infusing TRH directly into the dorsal raphe nucleus resembled those produced by icv infusion, and their magnitude diminished after pentolinium-induced ganglioplegia. These results are compatible with the interpretation that icv infused TRH may produce its cardiovascular and sympathetic effects by acting, at least in part, on serotonergic mechanisms located in the dorsal raphe nucleus.

摘要

在乌拉坦麻醉的大鼠中记录了对脑室内(icv)注入促甲状腺激素释放激素(TRH)的升压、心动过速和交感兴奋反应,以确定中枢给予的TRH在脑中的作用部位。内侧视前区、下丘脑后部或室旁核的电解损伤,或通过icv注入6-羟基多巴胺破坏儿茶酚胺能神经元所产生的化学损伤,均未改变这些反应。相比之下,当用5,7-二羟基色胺类似地破坏5-羟色胺能神经元时,TRH诱导的心动过速受到抑制。伴随的升压反应也被背侧中缝核而非中缝正中核的电解损伤所抑制。将TRH直接注入背侧中缝核所引发的升压和交感兴奋反应与icv注入所产生的反应相似,且在喷托铵诱导的神经节阻断后其幅度减小。这些结果符合这样的解释,即icv注入的TRH可能至少部分通过作用于位于背侧中缝核的5-羟色胺能机制来产生其心血管和交感效应。

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