Prenatal cocaine raises mu-opioid receptor density in piglet cardiorespiratory medulla.

Repeated prenatal exposure to cocaine attenuates arousal and cardiorespiratory functions in neonates. This study explored the possible role of brainstem mu- and delta-opioid systems in these effects. Medullary sections were obtained from 6 to 7 (young) and 20 to 21-day-old (older) piglets either unexposed or exposed prenatally to a 2-mg/kg intravenous cocaine hydrochloride dose, injected to the pregnant sow four times a day during the last third of gestation. Mu- and delta-opioid receptor binding was assessed by quantitative autoradiography using, respectively, 125I-DAMGO (Tyr-D-Ala-Gly-N-Me-Phe-Gly-ol) and 125I-DPDPE (Tyr-D-Pen-Gly-pCl-Phe-D-Pen). At control, delta-, but not mu-opioid, receptor density increased with postnatal age. In contrast, cocaine-induced mu-, but not delta-opioid, receptor density increased 1) in the dorsal motor vagal (dmnX) and facial (nF) nuclei, and, at borderline significance level, in the cardiorespiratory-related gigantocellular reticular nucleus (nRG) of the young, and 2) in the spinal trigeminal nucleus and tract (nSp5), and in the cardiorespiratory-related medial solitary tract (nTSm) and lateral reticular (nRL) nuclei of both age groups. These findings support a possible participation of the mu-opioid system in the attenuation of arousal and cardiorespiration after repeated prenatal exposure to cocaine.