Prenatal haloperidol alters striatal dopamine and opiate receptors.
Dopamine receptors were chronically blocked with haloperidol during prenatal development. The treatment resulted in a large decrease in [3H]naloxone binding to striatal opiate receptors and increased [3H]spiperone binding to dopamine receptors with these effects being apparent on the day of birth (P0). The autoradiographically visualized patterns of receptor distribution were unaltered. At 16 days, postnatally (P16), a period that marks the end of the postnatal spurt in brain growth, dopamine receptor binding was still elevated and opiate receptor binding was still diminished. The differential effect of haloperidol on the density and developmental time course of the dopamine and non-dopamine systems suggests that complex developmental interactions normally occur, and that these can be disrupted by maternal administration of neuroleptic drugs.
D000818:Animals; D003342:Corpus Striatum / Q000187:drug effects* / Q000196:embryology; D005260:Female; D006220:Haloperidol / Q000494:pharmacology*; D008431:Maternal-Fetal Exchange; D009270:Naloxone / Q000378:metabolism; D011247:Pregnancy; D051381:Rats; D011919:Rats, Inbred Strains; D011954:Receptors, Dopamine / Q000187:drug effects*; D011957:Receptors, Opioid / Q000187:drug effects*; D013134:Spiperone / Q000378:metabolism
D011954:Receptors, Dopamine; D011957:Receptors, Opioid; D009270:Naloxone; D013134:Spiperone; D006220:Haloperidol