Dopaminergic modulation of rat pup ultrasonic vocalizations

Abstract

The dopamine D 1 receptor agonist, R(+)-6-chloro-7,8-dihydroxy-1-phenyl-2,3,4,5-tetrahydro-1 H-3-benzazepine hydrobromide (SKF 81297), the dopamine D 2/D 3 receptor agonist, trans-(−)-4 aR-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.