title: Neonatal exposure to the D1 agonist SKF38393 inhibits pair bonding in the adult prairie vole.
abstract: The monogamous prairie vole displays developmental sensitivity to early pharmacological manipulation in a number of species-typical social behaviors. The long-term consequences of altering the neonatal dopamine system are not well characterized. This study examined whether early manipulation of the dopamine system, a known mediator of adult prairie vole social behavior, during neonatal development would affect adult aggressive and attachment behaviors. Eight-day-old pups were given a single treatment with either 1 mg/kg of SKF38393 (D1 agonist), quinpirole (D2 agonist), SCH23390 (D1 antagonist), eticlopride (D2 antagonist), or saline vehicle. As adults, animals received tests for intrasexual aggression and partner preference. Activation of D1-like receptors in pups impaired partner preference formation, but had no effect on aggression. Other neonatal treatments had no effect on their behavior as adults. To determine whether D1 activation in pups induced changes in dopamine receptor expression, we performed autoradiography on striatal tissue from a second cohort of saline-treated and SKF38393-treated animals. Although sex differences were observed, we found no treatment differences in D1 or D2 receptor binding in any striatal subregion. This study shows that exposure to a single early pharmacological alteration of dopamine receptor activity may have long-term effects on the social behavior of prairie voles.
authors.affiliation: Department of Psychology, University of California, Davis, CA, USA. caroline.hostetler@gmail.com
authors.forename: Caroline M
authors.initials: CM
authors.lastname: Hostetler
authors.forename: Shanna L
authors.initials: SL
authors.lastname: Harkey
authors.forename: Tarin B
authors.initials: TB
authors.lastname: Krzywosinski
authors.forename: Brandon J
authors.initials: BJ
authors.lastname: Aragona
authors.forename: Karen L
authors.initials: KL
authors.lastname: Bales
mesh_terms: D015647:2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine / Q000494:pharmacology*; D000367:Age Factors; D000374:Aggression; D000818:Animals; D000831:Animals, Newborn; D003411:Arvicolinae; D001522:Behavior, Animal / Q000187:drug effects*; D001552:Benzazepines; D015331:Cohort Studies; D003342:Corpus Striatum / Q000378:metabolism; D004298:Dopamine / Q000502:physiology; D018491:Dopamine Agonists / Q000494:pharmacology*; D018492:Dopamine Antagonists / Q000494:pharmacology; D065127:Dopamine D2 Receptor Antagonists; D005260:Female; D008297:Male; D017072:Neostriatum / Q000378:metabolism; D019257:Quinpirole / Q000494:pharmacology; D017447:Receptors, Dopamine D1 / Q000819:agonists / Q000037:antagonists & inhibitors; D017448:Receptors, Dopamine D2 / Q000819:agonists; D012457:Salicylamides / Q000494:pharmacology; D012737:Sex Factors; D012726:Sexual Behavior, Animal; D012919:Social Behavior
chemical_list: D001552:Benzazepines; D018491:Dopamine Agonists; D018492:Dopamine Antagonists; D065127:Dopamine D2 Receptor Antagonists; D017447:Receptors, Dopamine D1; D017448:Receptors, Dopamine D2; C534628:SCH 23390; D012457:Salicylamides; D019257:Quinpirole; D015647:2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine; C045989:eticlopride; D004298:Dopamine