THE DEVELOPMENT OF BETA(1)-ADRENOCEPTORS IN BROWN ADIPOSE-TISSUE FOLLOWING PRENATAL ALCOHOL EXPOSURE

Prenatal alcohol exposure delays the development of thermoregulation i n newborn rats. Newborns generate heat by the sympathetic nervous syst em's activation of nonshivering thermogenesis in brown adipose tissue (BAT). In this study, the effects of prenatal alcohol exposure on the development of the beta-adrenergic receptor system of BAT was investig ated by assessing the number and pharmacological properties of beta-ad renergic receptors in BAT in 1-, 5-, 10-, and 20-day-old offspring. Pr egnant dams were given either a liquid diet with 35% of the calories d erived from alcohol, a liquid diet without alcohol to control for any effects of the liquid diet administration, or ad lib food and water, O ffspring from the alcohol prenatal treatment group had a greater numbe r of beta(1) adrenergic receptors compared to offspring from both from the pair-fed and lab chow control groups, which did not differ from e ach other. The greater number of receptor sites in 5-day-old subjects suggests that the number of binding sites in alcohol-exposed BAT cells continues to rise due to the absence of sufficient neurotransmitter, and perhaps reflects a delay in the arrival of sympathetic nervous sys tem neurons. During the second and third postnatal weeks, when NE conc entrations are rising and reaching asymptotic levels, the number of be ta(1) adrenergic receptors in BAT of control subjects is decreasing. T his expected compensatory ''downregulation'' response in receptor conc entration was not seen in BAT from subjects exposed to alcohol prenata lly. These findings may have important implications for understanding the effects of prenatal alcohol exposure on developing plasticity in t he peripheral nervous system.