During development of the central nervous system, neurons pass through critical periods of vulnerability to environmental factors. Exposure to ethanol during gastrulation or during neuronal generation results in a permanent reduction in the number of neurons in trigeminal-associated cranial nerve nuclei. Normal functioning of the trigeminal system is required for social behavior, the present study examined the effects of acute prenatal exposure to ethanol on social interactions across ontogeny. Pregnant Long-Evans rats were injected with 2.9 g/kg ethanol (i.p., 20%, v/v solution; peak blood ethanol concentrations of ∼300 mg/dl) or an equivalent volume of saline on gestational day (G) 7 (gastrulation) or G12 (neuronal generation). Subsequently, social investigation, play fighting, contact behavior, social motivation, and overall locomotor activity in the social context were assessed in male and female off-spring during early adolescence, late adolescence, or adulthood, on postnatal day (P) 28, P42, or P75, respectively, using a modified social interaction test. Ethanol exposure on G7 resulted in mild changes of social behavior evident in young adolescents only. In contrast, animals exposed to ethanol on G12 demonstrated pronounced behavioral deficits throughout ontogeny, with deficits being most robust in male off-spring. Males exposed to ethanol on G12 showed decreases in social investigation, contact behavior, and play fighting, whereas a decrease in social motivation, i.e., transformation of social preference into social avoidance, was evident at P42 and P75 regardless of sex. These findings show that acute exposure to ethanol alters social behavior, and that the timing of the exposure defines the behavioral outcome.
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