Autoradiographic evidence that prenatal morphine exposure sex-dependently alters μ-opioid receptor densities in brain regions that are involved in the control of drug abuse and other motivated behaviors
Abstrakt
The present study examined the effects of prenatal morphine exposure on μ-opioid receptor density in young adult male and female rats to assess the long-term alterations in several brain areas including the nucleus accumbens (NAc), bed nucleus of stria terminalis (BNST), and the basolateral (BLA), lateral (LA), central (CeA), and posteromedial cortical (PMCoA) amygdaloid nuclei. These brain areas are involved in motivating and rewarding behaviors of opiates and other drugs of abuse.
The reinforcing actions of opiates appear to be μ-opioid receptor dependent. The results demonstrate that in male rats, prenatal morphine exposure significantly increases the density of μ-opioid receptors in the NAc and PMCoA.
In contrast, the same prenatal morphine exposure reduces the density of μ-opioid receptors in the BLA, while increasing it in the CeA and without effects in the LA or BNST. In female rats, prenatal morphine exposure has no effects on the density of μ-opioid receptors in the above six brain areas, but the density of these receptors is dependent on the presence or absence of ovarian hormones.
Thus, the present study demonstrates that mid- to late gestational morphine exposure induces long-term, sex-specific alterations in the density of μ-opioid receptors in the NAc and amygdala. Moreover, this prenatal morphine exposure also eliminates sex differences in the density of μ-opioid receptors in the NAc, CeA, and PMCoA but not in the BLA, LA, and BNST.