Abstract
Prenatal exposure to diazepam, a benzodiazepine (BZD) compound, leads to pronounced effects on responses to stressors in exposed animals when they reach adulthood. Many of the responses are sex specific. The mechanisms mediating the effects of the exposure on the organism have not been elucidated; however, the time course for the appearance of altered function following in utero drug exposure indicates that the exposure interfered with neural organization of mechanisms mediating responses to stressors. The article discusses possible mechanisms that relate to sites of action of the drug in the developing brain: the GABA A receptor, and the mitochondrial BZD receptor. The mechanisms mediating the sex-specific impact of diazepam on the developing brain appear to be complex and interactive.
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