Recent findings indicate that NSCs (specifically, in the dentate gyrus of the hippocampus and in the SVC of the anterior lateral ventricles) divide throughout life and give rise to new neurons. This observation has provided a new theoretical framework for understanding processes regulating brain plasticity. The factors that regulate neurogenesis overlap with those that are altered as alcohol use becomes alcoholism (e. g. , stress, activity, learning, and other unknown environmental and genetic factors).
Although the mechanisms involved are not well understood, it is possible that modulation of neurogenesis contributes significantly to alcoholic pathology. In animal models, high doses of alcohol have been shown to disrupt neurogenesis, and may underlie long-term deficits in hippocampal structure and function. More moderate but chronic alcohol consumption also affects neurogenesis, suggesting that inhibition of neurogenesis may contribute to the neurodegeneration associated with chronic alcoholism.
Alcohol may lead to disruptions in neurogenesis in several ways: through increased levels of glucocorticoids triggered by stress, direct inhibition of glutamate–NMDA receptors, serotonin dysregulation, and inhibition of growth factor-mediated cell proliferation. Research is needed to more directly determine the function of adult neurogenesis and how alcohol-induced inhibition of neurogenesis might contribute both to the pathology and the behavioral changes associated with alcohol abuse.