Alcohol, Corticosteroids, Energy Utilization, and Hippocampal Endangerment

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Abstract
The cellular weakening or cytoxic consequences of CAC are intertwined in the most fundamental sense with energy intake, production, storage, and mobilization. The impact of CAC on the HPA axis to increase GCs makes this energy regulatory hormone along with pancreatic hormones a potential major player in the site-specific organ pathologies associated with CAC. Although little is known about the mechanism of CAC neurotoxicity, the hippocampal endangerment model which relies heavily on the cellular weakening, site-specific effect of continuous or chronic, intermittent (withdrawal, binge drinking) elevation of GCs, even less is known about the mechanism of neurotoxicity of activating the ethanol-inducible CYP2E1 system. It is likely that components of both models contribute to the site-specific, CNS neurotoxicity associated with CAC, but this remains largely unresolved.