Sousa N, Madeira M D, Paula-Barbosa M M, Buijs R
Department of Anatomy, Porto Medical School, Portugal.
Brain Res. 1994 Jun 13;648(1):53-8. doi: 10.1016/0006-8993(94)91904-6.
We have recently reported that ethanol ingestion induces morphological changes in the vasopressinergic neurons of the supraoptic nucleus and that withdrawal from alcohol partially reverses these alterations. Since the production of vasopressin is not restricted to the magnocellular neurons of the hypothalamus, we investigated the effects of long-term ethanol intake and withdrawal on the lateral septum, an area heavily innervated by vasopressinergic fibers. Besides, as ethanol leads to a decrease of the plasma levels of testosterone, a hormone which plays a pivotal role in the development and maintenance of the vasopressinergic innervation of the lateral septum, we included groups of alcohol-fed animals submitted to testosterone replacement both in physiological and supraphysiological doses. In ethanol-treated rats there was a marked reduction in the number of vasopressin-immunoreactive fibers in the lateral septum. Following ethanol withdrawal a partial recovery in the number of vasopressin-immunoreactive fibers was observed. In both groups of ethanol + testosterone-treated animals the vasopressinergic innervation was increased when compared to the alcohol-fed group, although a complete reversal was not achieved. Therefore, two mechanisms might be regarded as underlying the impoverishment of the vasopressinergic innervation in the lateral septum after prolonged alcohol consumption: alcohol-induced cell death in the bed nucleus of the stria terminalis, from where these fibers arise, and/or alcohol-induced decrease in testosterone plasma levels.
我们最近报告称,摄入乙醇会引起视上核中加压素能神经元的形态变化,而戒酒可部分逆转这些改变。由于加压素的产生并不局限于下丘脑的大细胞神经元,我们研究了长期摄入乙醇及戒酒对外侧隔区的影响,该区域接受大量加压素能纤维的支配。此外,由于乙醇会导致血浆睾酮水平降低,而睾酮在外侧隔区加压素能神经支配的发育和维持中起关键作用,我们纳入了接受生理剂量和超生理剂量睾酮替代的乙醇喂养动物组。在乙醇处理的大鼠中,外侧隔区加压素免疫反应性纤维的数量显著减少。戒酒之后,观察到加压素免疫反应性纤维数量有部分恢复。与乙醇喂养组相比,两组乙醇 + 睾酮处理的动物的加压素能神经支配均有所增加,尽管未完全逆转。因此,长期饮酒后外侧隔区加压素能神经支配减少可能有两种潜在机制:乙醇诱导终纹床核(这些纤维的起源部位)中的细胞死亡,和/或乙醇诱导血浆睾酮水平降低。