Dopaminergic modulation of rat pup ultrasonic vocalizations.

F N Dastur, I S McGregor, R E Brown

Index: Eur. J. Pharmacol. 382 , 53, (1999)

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Abstract

The dopamine D(1) receptor agonist, R(+)-6-chloro-7, 8-dihydroxy-1-phenyl-2,3,4,5-tetrahydro-1H-3-benzazepine hydrobromide (SKF 81297), the dopamine D(2)/D(3) receptor agonist, trans-(-)-4aR-4,4a,5,6,7,8,8a,9-octahydro-5-propyl-1H-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-1H-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.