EFFECT OF NALTREXONE ON FEEDING, NEUROPEPTIDE-Y AND UNCOUPLING PROTEIN GENE-EXPRESSION DURING LACTATION

Neuropeptide Y increases feeding and decreases measures of brown adipo se tissue thermogenesis. In lactating rats, increased feeding, increas ed hypothalamic neuropeptide Y neuroactivity and decreased thermogenes is occur. Naltrexone is an opioid receptor antagonist which decreases neuropeptide Y-induced feeding and reverses neuropeptide Y-induced dec reases in brown adipose tissue thermogenesis. We hypothesized that opi oid receptors are involved in neuropeptide Y neuroactivity during lact ation. To see if naltrexone would alter feeding, neuropeptide Y gene e xpression in the arcuate nucleus, neuropeptide Y levels in the paraven tricular nucleus, and uncoupling protein gene expression in brown adip ose tissue of lactating rats, osmotic minipumps pre-filled with either 0.9% saline or naltrexone (70 mu g/h) were implanted subcutaneously i n 47 female Spraque-Dawley rats weighing 309+/-5g. Half these rats wer e studied on days 10-16 of lactation, and the other half were studied 7 days after lactation. After 48 h, neuropeptide Y mRNA levels and unc oupling protein MRNA levels were determined using specific cDNA probes . Neuropeptide Y peptide levels in the paraventricular nucleus were me asured by radioimmunoassay. Naltrexone decreased food intake by 26% in the post-lactating rats, but had no effect on feeding in the lactatin g animals. Lactation resulted in significantly increased arcuate neuro peptide Y mRNA, decreased neuropeptide Y levels in the paraventricular nucleus and decreased brown adipose tissue uncoupling protein mRNA le vels. Naltrexone did not influence any of these parameters. Thus, the alterations in neuropeptide Y neuroactivity and brown fat thermogenesi s which occur in lactation is not altered by generalized opioid recept or blockade.