Dopaminergic modulation of rat pup ultrasonic vocalizations

The dopamine D-1 receptor agonist, R(+)-6-chloro-7,8-dihydroxy-1-phenyl-2,3,4, H-3-benzazepine hydrobromide (SKF-81297), the dopamine D-2/D-3 receptor agonist, trans-( -)-4aR-4,4 a,5,6,7,8,8 a,9-octahydro-5-propyl- 1 H-pyrazolo[3,4-g]quinoline hydrochloride (quinpirole), and the dopamine D-3 receptor agonist, (+)-7-hydroxy-dipropylaminotetralin hydrobromide (7-OH-DPAT) all reduced the frequency of isolation-induced infant rat ultrasonic vocalizations and lowered body temperature when compared to saline-injected controls. Ultrasonic vocalization rate was not affected by either the dopamine D-1 receptor antagonist, R(+)-2,3,4,5-tetrahydro-8-iodo-3-methyl-5-phenyl- 1 H-3-benzazepin-7-ol hydrochloride (SCH 23390) or the dopamine D-2/D-3 receptor antagonist, S(-)-raclopride-L-tartrate (raclopride) when given alone, nor did these antagonists block the ultrasonic vocalization reductions caused by the dopamine D-1 receptor agonist or the dopamine D-2/D-3 receptor agonist. The dopamine D-2/D-3, receptor antagonist but not the dopamine D-1 receptor antagonist blocked the dopamine D-3 receptor agonist's ultrasonic vocalization reduction. SKF 81297 reduced general activity while quinpirole and 7-OH-DPAT increased activity. Raclopride reversed quinpirole's reduction in body temperature, as well as 7-OH-DPAT's effects on body temperature, ultrasonic vocalizations, and activity. These results indicate that dopamine D-1, D-2/D-3, and D-3 receptor agonists all reduce ultrasonic vocalizations by as yet undetermined mechanisms. (C) 1999 Elsevier Science B.V. All rights reserved.