Addiction biology
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A single exposure of infant rats or mice to ethanol during synaptogenesis (mid to late pregnancy for humans) can cause developing neurons to commit suicide (die by apoptosis) on a massive scale. The neuronal loss demonstrated in recent studies is more severe and much more widely distributed (many brain regions, plus spinal cord and retina) than has been documented in prior animal ethanol studies. By suppressing neuronal activity via NMDA glutamate and GABAA receptors, ethanol disrupts synaptogenesis, thereby activating in developing neurons a programmed signal to commit suicide. These recent findings help clarify important aspects of the fetal alcohol syndrome, and demonstrate the usefulness of an in vivo infant rodent model for studying the neurotoxic effects of ethanol on the developing central nervous system.
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Prenatal alcohol exposure can result in fetal alcohol syndrome (FAS), which may increase the risk of confinement in the corrections system. In the United States each state and four major cities' corrections systems were asked to complete a questionnaire on the prevalence of FAS and alcohol-related neurodevelopmental disorder (ARND) in the offender population, the availability of screening and diagnostic services to identify offenders with FAS and staff training needs related to FAS. The total population in the 54 entities was 3,080,904 inmates. ⋯ Reported staff training needs were very large. In conclusion, corrections systems have high unmet needs to screen, identify, and treat offenders with FAS and ARND. Staff training needs are substantial.