Andreae L C, Herbert J
Department of Anatomy, University of Cambridge, U.K.
Neuroscience. 1993 Apr;53(3):735-48. doi: 10.1016/0306-4522(93)90620-u.
Vasopressin has been shown to be localized in specific central nervous system (CNS) sites. There is considerable evidence that it can act as a central neurotransmitter and it has been ascribed a variety of putative roles in the CNS. To identify those regions of the brain capable of responding to this peptide, 250 pmol vasopressin were infused into the lateral ventricle intracerebroventricular of conscious, handled male rats, and their brains processed for fos-immunohistochemistry 60 min later. Increases in fos-immunoreactivity, compared with cerebrospinal fluid-infused controls, were found in specific regions of the basal forebrain and brainstem: the central nucleus of the amygdala, ventrolateral septum, parvocellular divisions of the paraventricular nucleus of the hypothalamus, dorsal tuberal nucleus and locus coeruleus. Pre-infusion of 2500 pmol of a V1a antagonist prevented or reduced the expression of c-fos by intracerebroventricular vasopressin in all areas except the dorsal parvocellular paraventricular nucleus, implying that in most (but not all) areas the actions of vasopressin are mediated by the V1a receptor. Central administration of vasopressin had no effect on plasma corticosterone levels. Vasopressin and corticotropin-releasing factor act synergistically on the anterior pituitary to cause release of adrenocorticotropic releasing hormone and have corresponding synergistic interactions on behaviour. Infusion of 250 pmol corticotropin releasing factor produced a similar but not identical pattern of fos-like immunoreactivity to that of vasopressin. Activation of the parabrachial nucleus was observed, but there was no significant effect on the lateral septum and apparent increases in the medial parvocellular division of the paraventricular nucleus and locus coeruleus were not significant. Corticotropin releasing factor also caused a marked rise in plasma corticosterone. When the two peptides were infused together (125 pmol each) no evidence for synergy was found, in terms of the number of neurons activated to express c-fos. The induction of differential patterns of fos-like immunoreactivity by vasopressin and corticotropin-releasing factor in specific regions of the limbic forebrain and brainstem has implications for the individual roles they play in the CNS.
血管加压素已被证明定位于特定的中枢神经系统（CNS）部位。有大量证据表明它可作为一种中枢神经递质，并且在中枢神经系统中被赋予了多种假定的作用。为了确定大脑中能够对这种肽产生反应的区域，将250皮摩尔血管加压素注入清醒、经过处理的雄性大鼠的侧脑室脑室内，60分钟后对其大脑进行Fos免疫组织化学处理。与注入脑脊液的对照组相比，在前脑基底和脑干的特定区域发现Fos免疫反应性增加：杏仁核中央核、腹外侧隔区、下丘脑室旁核小细胞部、背侧结节核和蓝斑。预先注入2500皮摩尔的V1a拮抗剂可预防或减少除室旁核背侧小细胞部外所有区域的脑室内血管加压素诱导的c-Fos表达，这意味着在大多数（但不是所有）区域，血管加压素的作用是由V1a受体介导的。中枢给予血管加压素对血浆皮质酮水平没有影响。血管加压素和促肾上腺皮质激素释放因子在前垂体上协同作用，导致促肾上腺皮质激素释放激素的释放，并在行为上有相应的协同相互作用。注入250皮摩尔促肾上腺皮质激素释放因子产生了与血管加压素相似但不完全相同的Fos样免疫反应模式。观察到臂旁核被激活，但对外侧隔区没有显著影响，室旁核内侧小细胞部和蓝斑的明显增加也不显著。促肾上腺皮质激素释放因子也导致血浆皮质酮显著升高。当将这两种肽一起注入（各125皮摩尔）时，就激活表达c-Fos的神经元数量而言，未发现协同作用的证据。血管加压素和促肾上腺皮质激素释放因子在边缘前脑和脑干的特定区域诱导不同模式的Fos样免疫反应性，这对它们在中枢神经系统中所起的个体作用具有启示意义。
