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室旁核介导去甲肾上腺素注射到背侧穹窿周区域引起的升压反应。

Paraventricular nucleus mediates pressor response to noradrenaline injection into the dorsal periaqueductal gray area.

机构信息

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

出版信息

Auton Neurosci. 2009 Dec 3;151(2):74-81. doi: 10.1016/j.autneu.2009.06.005. Epub 2009 Jun 28.

Abstract

The dorsal periaqueductal gray area (dPAG) is involved in cardiovascular modulation. In a previous study, we reported that noradrenaline (NA) microinjection into the dPAG of rats caused pressor response that was mediated by vasopressin release. Vasopressin is synthesized by magnocellular neurons in the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei. In the present study, we verified which nuclei mediated the cardiovascular response to NA as well as the existence of direct neural projection from the dPAG to hypothalamic nuclei. Then, we studied the effect of treating either PVN or SON with the nonselective synaptic blocker cobalt chloride (1mM) on the cardiovascular response to NA (15 nmol) microinjection into dPAG. Attempting to identify neural projections from dPAG to hypothalamic nuclei, we microinjected the neuronal tracer biotinylated-dextran-amine (BDA) into the dPAG and searched varicosity-containing nerve terminals in the PVN and SON. Unilateral cobalt-induced inhibition of synapses in the SON did not affect the cardiovascular response to NA. However, unilateral inhibition of PVN significantly reduced the pressor response to NA. Moreover, cobalt-induced inhibition of synapses in both PVN blocked the pressor response caused by NA microinjected into the dPAG. Microinjection of BDA into the dPAG evidenced presence of varicosity-containing neuronal fibers in PVN but not in SON. The results from cobalt treatment indicated that synapses in PVN mediate the vasopressin-induced pressor response caused by NA microinjection into the dPAG. In addition, the neuroanatomical results from BDA microinjection into the dPAG pointed out the existence of direct neural projections from the dPAG site to the PVN.

摘要

背侧periaqueductal 灰色区域 (dPAG) 参与心血管调节。在之前的研究中,我们报道了向大鼠的 dPAG 中微注射去甲肾上腺素 (NA) 会引起升压反应,该反应是通过血管加压素释放介导的。血管加压素由下丘脑室旁核 (PVN) 和视上核 (SON) 中的大细胞神经元合成。在本研究中,我们验证了哪些核介导了对 NA 的心血管反应,以及 dPAG 与下丘脑核之间是否存在直接的神经投射。然后,我们研究了用非选择性突触阻滞剂氯化钴 (1mM) 处理 PVN 或 SON 对 dPAG 中 NA (15 nmol) 微注射引起的心血管反应的影响。为了确定从 dPAG 到下丘脑核的神经投射,我们将神经元示踪剂生物素化葡聚糖胺 (BDA) 微注射到 dPAG 中,并在 PVN 和 SON 中寻找含有轴突终末的神经终末。单侧钴诱导的 SON 突触抑制不影响 NA 引起的心血管反应。然而,单侧 PVN 抑制显著降低了对 NA 的升压反应。此外,双侧 PVN 中的钴诱导的突触抑制阻断了 NA 微注射到 dPAG 引起的升压反应。将 BDA 微注射到 dPAG 中,证明了含有轴突终末的神经元纤维存在于 PVN 中,但不存在于 SON 中。钴处理的结果表明,PVN 中的突触介导了由 dPAG 中 NA 微注射引起的血管加压素诱导的升压反应。此外,从 BDA 微注射到 dPAG 的神经解剖学结果指出,dPAG 部位与 PVN 之间存在直接的神经投射。

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