
This report summarizes the proceedings of the symposium VII on the role of  neuroactive steroids in stress/alcohol interactions.
The production of GABAergic  neuroactive steroids, including (3α,5α)-3-hydroxypregnan-20-one and  (3α,5α)-3,21-dihydroxypregnan-20-one is a consequence of both acute stress and  acute ethanol exposure. Acute, but not chronic ethanol administration elevates  brain levels of these steroids and enhances GABAA receptor activity.  Neuroactive steroids modulate acute anticonvulsant effects, sedation, spatial  memory impairment, anxiolytic-like, antidepressant-like, and reinforcing  properties of ethanol in rodents.
Furthermore, these steroids participate in the  homeostatic regulation of the hypothalamic–pituitary–adrenal axis. Therefore, it  is not surprising that neuroactive steroids are involved in ethanol/stress  interactions. Nevertheless, the interactions are complex and not well  understood.
This symposium addressed the role of neuroactive steroids in both  stress and alcohol responses and their interactions. Professor Giovanni Biggio  of the University of Cagliari, Italy presented the effects of juvenile isolation  stress on neuroactive steroids, GABAA receptor expression, and  ethanol sensitivity.
Professor Howard Becker of the Medical University of South  Carolina, USA presented evidence for neuroactive steroid involvement in ethanol  dependence and drinking behavior.
Professor Patrizia Porcu of the University of  North Carolina, USA described a potential neuroactive steroid biomarker that may  predict heavy drinking in monkeys and mice.
These presentations provide a  framework for new theories on the nature of ethanol/stress interactions that may  be amenable to therapeutic interventions.
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