title: Dopamine's role in social modulation of infant isolation-induced vocalization: II. Maternally modulated infant separation responses are regulated by D1- and D2-family dopamine receptors.
abstract: Mammalian infant behavior directed toward caregivers is critical to survival and may play a role in establishing social bonds. Most mammalian infants vocalize when isolated. Rat pups vocalize at a higher rate when isolated following an interaction with an adult female than after an interaction with littermates, a phenomenon termed maternal potentiation. We previously reported that the D2 receptor family agonist quinpirole disrupts maternal potentiation at a dose that does not alter vocalization rate following contact with littermates. Here we further examine the role of dopamine in maternal potentiation by testing effects of both D1 and D2 receptor family ligands, alone and in combination, on maternal potentiation. We tested the drugs' effects on isolation vocalization subsequent to littermate contact and then another isolation preceded by a brief "reunion" period of exposure either to the anesthetized dam or a handling-only "pickup" condition. D2 receptor stimulation blocked the increase in vocalizations following reunion with the dam. The D2 agonist effect in the dam-reunion condition was much larger than its small effect in the pickup condition, providing further evidence that D2 receptors exert a selective modulation of maternal potentiation. On the other hand, systemic administration of the D1 agonist SKF81297 reduced isolation vocalizations nonspecifically, across all the experimental conditions. Finally, the D1 and D2 receptor dual antagonist, alpha-flupenthixol, increased isolation vocalizations and disrupted potentiation, but at doses that also inhibited locomotion. We conclude that D2 receptor family activation has a more selective effect of disrupting maternal potentiation than D1 receptor family activation.
authors.affiliation: Division of Developmental Neuroscience, New York State Psychiatric Institute, 1051 Riverside Drive, Unit 40, New York, NY 10032, USA. mullerj@pi.cpmc.columbia.edu
authors.forename: Jeff M
authors.initials: JM
authors.lastname: Muller
authors.forename: Holly
authors.initials: H
authors.lastname: Moore
authors.forename: Michael M
authors.initials: MM
authors.lastname: Myers
authors.forename: Harry N
authors.initials: HN
authors.lastname: Shair
mesh_terms: D000818:Animals; D004298:Dopamine / Q000502:physiology*; D018491:Dopamine Agonists / Q000008:administration & dosage / Q000494:pharmacology; D005260:Female; D008297:Male; D009035:Mothers / Q000523:psychology*; D019257:Quinpirole / Q000008:administration & dosage / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D017447:Receptors, Dopamine D1 / Q000187:drug effects / Q000502:physiology*; D017448:Receptors, Dopamine D2 / Q000187:drug effects / Q000502:physiology*; D012919:Social Behavior; D012934:Social Isolation; D014828:Vocalization, Animal; D014886:Weaning
chemical_list: D018491:Dopamine Agonists; D017447:Receptors, Dopamine D1; D017448:Receptors, Dopamine D2; D019257:Quinpirole; D004298:Dopamine