Baek J K, Heaton M B, Walker D W
Gainesville Veterans Administration Medical Center.
Alcohol Clin Exp Res. 1994 Dec;18(6):1368-76. doi: 10.1111/j.1530-0277.1994.tb01438.x.
Chronic ethanol treatment induces memory deficits accompanied by anatomical and biochemical changes in basal forebrain and hippocampus. Cholinergic neurons in the septohippocampal pathway are especially vulnerable to alcohol neurotoxicity. Several studies showed that an adequate supply of neurotrophins, such as Nerve Growth Factor and Brain-Derived Neurotrophic Factor, is required for the normal function and survival of cholinergic neurons in basal forebrain and medial septal nuclei. We tested the hypothesis that chronic alcohol ingestion may alter the gene expression level of Nerve Growth Factor in hippocampus, the major source of neurotrophins to the cholinergic neurons in the septohippocampal pathway. We measured Nerve Growth Factor protein and Nerve Growth Factor mRNA contents using sensitive two-site ELISA and Northern analysis. We also tested the endogenous neurotrophic activity, including and excluding Nerve Growth Factor, contained in 5%, 2%, 1%, 0.5% and 0.1% (w/v) hippocampal tissue extracts on sympathetic ganglia neurons. Twenty-eight weeks of chronic ethanol treatment did not reduce Nerve Growth Factor protein, Nerve Growth Factor mRNA, or total neurotrophic activity contained in the rat hippocampus when measured on sympathetic ganglia neurons.
慢性乙醇处理会导致记忆缺陷，并伴有基底前脑和海马体的解剖学和生物化学变化。隔海马通路中的胆碱能神经元尤其易受酒精神经毒性的影响。多项研究表明，充足的神经营养因子供应，如神经生长因子和脑源性神经营养因子，对于基底前脑和内侧隔核中胆碱能神经元的正常功能和存活是必需的。我们检验了这样一个假设，即长期摄入酒精可能会改变海马体中神经生长因子的基因表达水平，而海马体是隔海马通路中胆碱能神经元神经营养因子的主要来源。我们使用灵敏的双位点酶联免疫吸附测定法和Northern分析来测量神经生长因子蛋白和神经生长因子信使核糖核酸的含量。我们还测试了5%、2%、1%、0.5%和0.1%（w/v）海马体组织提取物中所含的内源性神经营养活性，包括和排除神经生长因子对交感神经节神经元的影响。当对交感神经节神经元进行测量时，28周的慢性乙醇处理并未降低大鼠海马体中神经生长因子蛋白、神经生长因子信使核糖核酸或总的神经营养活性。
