Department of Pharmacology, School of Medicine of Ribeirão Preto, University of São Paulo, Brazil.
Neuroscience. 2012 Sep 6;219:157-65. doi: 10.1016/j.neuroscience.2012.05.051. Epub 2012 May 28.
The medial amygdaloid nucleus (MeA) is a part of the limbic system and is involved in cardiovascular modulation. We previously reported that microinjection of noradrenaline (NA) into the MeA of unanesthetized rats caused pressor and bradycardiac responses, which were mediated by acute vasopressin release into the systemic circulation. In the present study, we tested the possible involvement of magnocellular neurons of the paraventricular (PVN) and/or supraoptic (SON) of the hypothalamus that synthesize vasopressin in the cardiovascular pathway activated by the microinjection of NA into the MeA. Pressor and bradycardiac responses to the microinjection of NA (27 nmol/100 nL) into the MeA were blocked by pretreatment of either the PVN or the SON with cobalt chloride (CoCl(2), 1 mM/100 nL), thus indicating that both hypothalamic nuclei mediate the cardiovascular responses evoked by microinjection of NA into the MeA. Our results suggest that the pressor and bradycardiac response caused by the microinjection of NA into the MeA is mediated by magnocellular neurons in both the PVN and SON.
内侧杏仁核(MeA)是边缘系统的一部分,参与心血管调节。我们之前的报告显示,在未麻醉大鼠的 MeA 中微注射去甲肾上腺素(NA)会引起升压和心动过缓反应,这是由急性血管加压素释放到体循环中介导的。在本研究中,我们测试了在 MeA 中微注射 NA 激活的心血管途径中,可能涉及合成血管加压素的下丘脑室旁核(PVN)和/或视上核(SON)的大细胞神经元的参与。用氯化钴(CoCl(2),1mM/100nL)预处理 PVN 或 SON,可阻断微注射 NA(27nmol/100nL)到 MeA 引起的升压和心动过缓反应,这表明这两个下丘脑核均介导微注射到 MeA 的 NA 引起的心血管反应。我们的结果表明,MeA 中微注射 NA 引起的升压和心动过缓反应是由 PVN 和 SON 中的大细胞神经元介导的。