Chronic alcohol ingestion: nerve growth factor gene expression and neurotrophic activity in rat hippocampus

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.