Persisting subsensitivity of the striatal dopamine system after fetal exposure to beta-endorphin.

Overview

Fetal exposure of rats to beta-endorphin during the third trimester, either alone or with alpha-MSH, resulted in mild developmental delay and significant decreases in striatal dopamine receptor density (subsensitivity) persisting through maturity. The apparent paradoxical down-regulation of dopamine receptors in the presence of beta-endorphin was consistent with fetal exposure to dopamine receptor antagonists and synthesis inhibitors. These findings suggest biophysical properties of receptors which are unique to fetal development including loss of plasticity after exposure to antagonists. Permanent, down-regulation of the striatal dopamine system may be one mechanism underlying delayed development after fetal exposure to beta-endorphin which may accompany hypoxia. Even though there were no statistically significant differences between males and females in density of the dopamine receptor, the behavioral profile after peptide treatment was sexually demorphic. Behaviorally, female rats appeared sensitized to perinatal alpha-MSH and males to alpha-endorphin.