title: Increased sensitivity of dopamine systems following reproductive experience in rats.
abstract: Several studies have suggested that alterations in forebrain dopamine activity during the postpartum period may result in the onset of postpartum psychosis in women [J. Psychosom. Obstet. Gynecol. 19 (1998) 104; Prog. Neuro-Psychopharmacol. Biol. Psychiatry 17 (1993) 571; J. Clin. Psychiatry 51 (1990) 365.]. The present study investigated whether increased dopamine activity in these forebrain regions is a normal consequence of reproductive experience in rodents. Both intact and ovariectomized parous and nulliparous females were tested for their responses to the dopamine agonist apomorphine using two behavioral measures, prepulse inhibition (PPI) and oral stereotypy. In addition, dopamine and DOPAC levels were measured in tissue from the striatum and nucleus accumbens together with circulating plasma prolactin levels. The results of the behavioral studies demonstrate an increased response to apomorphine in parous females. Parous subjects also had increased levels of dopamine and DOPAC in striatal tissue and lower levels of circulating prolactin. Ovariectomy in nulliparous females resulted in a potentiated response to apomorphine with regard to the disruption of PPI, as well as a significant decrease in the plasma prolactin levels, as compared with intact nulliparous females. These data suggest that increased dopamine activity in forebrain regions occurs as a consequence of parity, which persists for a minimum of several weeks postpartum. These findings support the hypothesis that increased dopamine sensitivity in forebrain dopamine regions may be one potential mechanism underlying the development of postpartum psychosis in women.
authors.affiliation: Department of Biomedical Sciences, Tufts University School of Veterinary Medicine, 200 Westboro Road, North Grafton, MA 01536, USA.
authors.forename: E M
authors.initials: EM
authors.lastname: Byrnes
authors.forename: J J
authors.initials: JJ
authors.lastname: Byrnes
authors.forename: R S
authors.initials: RS
authors.lastname: Bridges
mesh_terms: D000818:Animals; D003216:Conditioning, Operant / Q000187:drug effects; D003913:Dextroamphetamine / Q000494:pharmacology; D004193:Discrimination Learning / Q000187:drug effects; D018491:Dopamine Agonists / Q000494:pharmacology*; D018492:Dopamine Antagonists / Q000494:pharmacology; D018765:Dopamine Uptake Inhibitors / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D005795:Generalization, Stimulus / Q000187:drug effects; D008297:Male; D019257:Quinpirole / Q000494:pharmacology*; D051381:Rats; D020318:Rats, Long-Evans; D017447:Receptors, Dopamine D1 / Q000819:agonists; D017448:Receptors, Dopamine D2 / Q000819:agonists; D050637:Receptors, Dopamine D3; D017981:Receptors, Neurotransmitter / Q000187:drug effects*; D017661:Receptors, Presynaptic / Q000187:drug effects; D013764:Tetrahydronaphthalenes / Q000494:pharmacology*
chemical_list: D018491:Dopamine Agonists; D018492:Dopamine Antagonists; D018765:Dopamine Uptake Inhibitors; C493595:Drd3 protein, rat; D017447:Receptors, Dopamine D1; D017448:Receptors, Dopamine D2; D050637:Receptors, Dopamine D3; D017981:Receptors, Neurotransmitter; D017661:Receptors, Presynaptic; D013764:Tetrahydronaphthalenes; D019257:Quinpirole; C031349:7-hydroxy-2-N,N-dipropylaminotetralin; D003913:Dextroamphetamine