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涉及去甲肾上腺素在外侧隔区对心血管反应调制作用的脑内通路。

Brain pathways involved in the modulatory effects of noradrenaline in lateral septal area on cardiovascular responses.

机构信息

Department of Pharmacology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil.

出版信息

Cell Mol Neurobiol. 2012 Oct;32(7):1147-57. doi: 10.1007/s10571-012-9840-4. Epub 2012 Apr 7.

Abstract

We have previously reported that stimulation of alpha-1 adrenoceptors by noradrenaline (NA) injected into the lateral septal area (LSA) of anaesthetized rats causes pressor and bradycardic responses that are mediated by acute vasopressin release into the circulation through activation of the paraventricular nucleus (PVN). Although the PVN is the final structure of this pathway, the LSA has no direct connections with the PVN, suggesting that other structures may connect these areas. To address this issue, the present study employed c-Fos immunohistochemistry to investigate changes caused by NA microinjection into the LSA in neuronal activation in brain structures related to systemic vasopressin release. NA microinjected in the LSA caused pressor and bradycardic responses, which were blocked by intraseptal administration of α-1 adrenoceptor antagonist (WB4101, 10 nmol/200 nL) or systemic V-1 receptor antagonist (dTyr(CH2)5(Me)AVP, 50 μg/kg). NA also increased c-Fos immunoreactivity in the prelimbic cortex (PL), infralimbic cortex (IL), dorsomedial periaqueductal gray (dmPAG), bed nucleus of the stria terminalis (BNST), PVN, and medial amygdala (MeA). No differences in the diagonal band of Broca, cingulate cortex, and dorsolateral periaqueductal gray (dlPAG) were found. Systemic administration of the vasopressin receptor antagonist dTyr AVP (CH2)5(Me) did not change the increase in c-Fos expression induced by intra-septal NA. This latter effect, however, was prevented by local injection of the alpha-1 adrenoceptor antagonist WB4101. These results suggest that areas such as the PL, IL, dmPAG, BNST, MeA, and PVN could be part of a circuit responsible for vasopressin release after activation of alpha-1 adrenoceptors in the LSA.

摘要

我们之前曾报道过,在麻醉大鼠的侧隔区(LSA)注射去甲肾上腺素(NA)刺激α-1 肾上腺素受体,会引起加压和心动过缓反应,这是通过激活室旁核(PVN)将急性血管加压素释放到循环中介导的。尽管 PVN 是该途径的最终结构,但 LSA 与 PVN 没有直接联系,这表明其他结构可能连接这些区域。为了解决这个问题,本研究采用 c-Fos 免疫组织化学方法,研究了 NA 微注射到 LSA 引起的与全身血管加压素释放有关的脑结构中神经元激活的变化。NA 微注射到 LSA 会引起加压和心动过缓反应,这些反应被 LSA 内给予 α-1 肾上腺素受体拮抗剂(WB4101,10 nmol/200 nL)或全身 V-1 受体拮抗剂(dTyr(CH2)5(Me)AVP,50 μg/kg)阻断。NA 还增加了前扣带回皮层(PL)、下边缘皮层(IL)、背内侧导水管周围灰质(dmPAG)、终纹床核(BNST)、PVN 和内侧杏仁核(MeA)中的 c-Fos 免疫反应性。在 Broca 斜带、扣带回皮层和背外侧导水管周围灰质(dlPAG)中没有发现差异。全身给予血管加压素受体拮抗剂 dTyr AVP(CH2)5(Me) 不会改变内隔 NA 引起的 c-Fos 表达增加。然而,这种效应被局部注射 α-1 肾上腺素受体拮抗剂 WB4101 所阻止。这些结果表明,PL、IL、dmPAG、BNST、MeA 和 PVN 等区域可能是激活 LSA 中的 α-1 肾上腺素受体后导致血管加压素释放的回路的一部分。

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