The effects of chronic postweaning amphetamine on rats exposed to alcohol in utero: weight gain and behavior
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Published on: July 13, 2014
1Department of Obstetrics and Gynecology, Wayne State University School of Medicine, Detroit, MI 48201.
Insights
Prenatal alcohol exposure in rats affects amphetamine response, influencing locomotor activity and sensitization in males. This suggests potential differences in how children with Fetal Alcohol Syndrome may respond to stimulant medications.
Area of Science:
- Neuroscience
- Developmental Psychology
- Pharmacology
Background:
- Prenatal alcohol exposure can lead to Fetal Alcohol Syndrome (FAS), impacting neurodevelopment.
- Central nervous system (CNS) stimulants are sometimes used to manage attentional deficits in FAS.
Purpose of the Study:
- To investigate the long-term effects of prenatal alcohol exposure on behavioral responses to amphetamine in rats.
- To determine if prenatal alcohol exposure alters growth and behavioral sensitivity to amphetamine in offspring.
Main Methods:
- Rats exposed to alcohol in utero were administered amphetamine daily from postnatal day 22 to 42.
- Body weight and behavioral responses (locomotor activity, stereotypy, catalepsy) were measured at various postnatal days.
Main Results:
- Prenatal alcohol exposure resulted in lower birth weight but accelerated weight gain during amphetamine treatment.
- Alcohol-exposed rats showed increased locomotor activation to amphetamine (2 mg/kg).
- Male rats exposed to alcohol prenatally exhibited amphetamine sensitization, unlike controls.
Conclusions:
- Prenatal alcohol exposure alters offspring's response to amphetamine, particularly locomotor activation and sensitization in males.
- These findings suggest that individuals with FAS may exhibit varied dose-responses to CNS stimulants for behavioral effects, but not necessarily for growth-related side effects.
Abstract:
Offspring of rats fed alcohol, pair-fed, or fed ad lib control diets during pregnancy were administered a dose of amphetamine (0, 2 or 10 mg/kg) daily from postnatal day 22 (PN22) to PN42. Body weight was measured regularly from PN22 to PN60, and behavior was measured on PN22, PN28, PN36 and PN42. Rats exposed to alcohol in utero weighed less than controls at birth and throughout most of the experiment, despite a significantly accelerated weight gain relative to controls. By PN60, prenatal alcohol-exposed rats weighed the same as pair-fed controls. There were dose-dependent reductions in the rate of weight gain during amphetamine administration. After the daily injections stopped, the high-dose (10-mg/kg) amphetamine groups showed a higher growth rate than the 0-mg/kg and 2-mg/kg groups. There were no interactions between prenatal treatment and dose of amphetamine on body weight gain. Rats exposed to alcohol in utero showed a greater locomotor activation than controls given 2 mg/kg amphetamine. The magnitude of the locomotor activation to this dose of amphetamine decreased equivalently over the four test days for all prenatal treatment groups. Male but not female rats exposed prenatally to alcohol showed an apparent sensitization to 10 mg/kg amphetamine not seen in control rats between PN28 and PN42. There were no group differences in amphetamine-induced stereotypy or SCH-23390-induced catalepsy. The results implied that children with Fetal Alcohol Syndrome who may be treated for attentional dysfunction would show different dose-responses for some behavioral effects of CNS stimulants, but not for growth-retarding "side effects."
