Sivukhina E V, Dolzhikov A A, Morozov Iu E, Jirikowski G F, Grinevich V
Department of Anatomy II, Friedrich Schiller University, Jena, Germany.
Horm Metab Res. 2006 Jun;38(6):382-90. doi: 10.1055/s-2006-944522.
Although numerous data showing severe morphological impairment of magnocellular and parvocellular hypothalamic neurons due to chronic alcoholic consumption have been gathered from animal experiments, only one study (Harding et al., 1996) was performed on POST MORTEM human brain. This study showed a reduction in the number of vasopressin (VP)-immunoreactive neurons in the supraoptic (SON) and paraventricular (PVN) nuclei, but did not provide any data regarding the effect of chronic alcohol intake on human parvocellular neurons. In order to assess whether the changes observed in the animal model also occur in humans and provide a structural basis for the results of clinical tests, we performed immunohistochemical and morphometric analysis of magnocellular (VP and oxytocin, OT) and parvocellular (corticotropin-releasing hormone, CRH) neurons in post-mortem brains of patients afflicted with chronic alcoholic disease. We analyzed 26-male alcoholics and 22 age-matched controls divided into two age groups--"young" (< 40 yr) and "old" (> 40 yr). Hypothalamic sections were stained for OT, VP, and CRH. The analysis revealed: 1) decrease in VP-immunoreactivity in the SON and PVN as well as OT-immunoreactivity in the SON in alcoholic patients; 2) increase in OT-immunoreactivity in the PVN; 3) increase in CRH-immunoreactivity in parvocellular neurons in the PVN. Furthermore, the proportion of cells containing CRH and VP was increased in alcoholics. These findings indicate that chronic alcohol consumption does indeed impair the morphology of magnocellular neurons. The enhancement of CRH-immunoreactivity and increased co-production of CRH and VP in parvocellular neurons may be due to a decline in glucocorticoid production, implied by the hypoplasic impairment of adrenal cortex we observed in alcoholics during the course of this study.
尽管从动物实验中已收集到大量数据，表明长期饮酒会导致下丘脑大细胞和小细胞神经元出现严重的形态学损伤，但仅一项研究（Harding等人，1996年）是针对人类尸检大脑进行的。该研究显示，视上核（SON）和室旁核（PVN）中血管加压素（VP）免疫反应性神经元数量减少，但未提供任何关于长期饮酒对人类小细胞神经元影响的数据。为了评估在动物模型中观察到的变化是否也会在人类中出现，并为临床测试结果提供结构基础，我们对患有慢性酒精性疾病患者的尸检大脑中的大细胞（VP和催产素，OT）和小细胞（促肾上腺皮质激素释放激素，CRH）神经元进行了免疫组织化学和形态计量分析。我们分析了26名男性酗酒者和22名年龄匹配的对照者，他们被分为两个年龄组——“年轻”（<40岁）和“年老”（>40岁）。下丘脑切片用OT、VP和CRH进行染色。分析结果显示：1）酗酒患者SON和PVN中VP免疫反应性降低，SON中OT免疫反应性降低；2）PVN中OT免疫反应性增加；3）PVN中小细胞神经元中CRH免疫反应性增加。此外，酗酒者中含有CRH和VP的细胞比例增加。这些发现表明，长期饮酒确实会损害大细胞神经元的形态。小细胞神经元中CRH免疫反应性的增强以及CRH和VP共同产生的增加可能是由于糖皮质激素分泌减少所致，在本研究过程中我们观察到酗酒者肾上腺皮质发育不全损伤提示了这一点。
