Aloe L, Tirassa P
Instituto di Neurobiologia, Consiglio Nazionale delle Ricerche, Rome, Italy.
Alcohol. 1992 Jul-Aug;9(4):299-304. doi: 10.1016/0741-8329(92)90070-q.
It was reported that chronic exposure to ethanol causes a loss of hippocampal pyramidal cells and of brain cholinergic neurons in both laboratory animals and humans. In the present study, it was hypothesized that nerve growth factor (NGF), a trophic agent for the survival and maintenance of basal forebrain cholinergic neurons (FCN), might be affected by the neurodegenerative events which occur during ethanol consumption. To test this hypothesis, we used aged rats (14 months) exposed for 16 weeks to 40 g/kg per day of undiluted wine. Our experiments showed that chronic alcohol consumption causes a reduction of NGF in the hippocampus (HI) and of choline acetyltransferase (ChAT) activity in both the septum and the HI and a reduction in the distribution of NGF-receptors (NGF-R) in the septum and nucleus of Meynert. Intracerebral injection of NGF in alcohol-exposed rats results in a return to normal levels of ChAT enzymatic activity and NGF-R expression. These experiments indicate that the damaging effect of alcohol on the FCN is also associated with impairment of central NGF-target structures.
据报道，长期接触乙醇会导致实验动物和人类的海马锥体细胞以及脑胆碱能神经元丧失。在本研究中，我们推测神经生长因子（NGF），一种对基底前脑胆碱能神经元（FCN）的存活和维持起营养作用的因子，可能会受到乙醇摄入过程中发生的神经退行性事件的影响。为了验证这一假设，我们使用了14个月大的大鼠，将其每天暴露于40克/千克未稀释的葡萄酒中，持续16周。我们的实验表明，长期饮酒会导致海马体（HI）中NGF减少，隔区和HI中胆碱乙酰转移酶（ChAT）活性降低，以及隔区和迈内特核中NGF受体（NGF-R）分布减少。对酒精暴露大鼠进行脑内注射NGF可使ChAT酶活性和NGF-R表达恢复到正常水平。这些实验表明，酒精对FCN的损害作用也与中枢NGF靶结构的损伤有关。
