Ultrasonic vocalizations of preweanling rats: involvement of both α 2-adrenoceptor and κ-opioid receptor systems

Abstract

Stimulation of α 2-adrenoceptors and κ-opioid receptors increases the ultrasonic vocalizations of preweanling rats. The purpose of the present study was to determine whether α 2-adrenoceptors and κ-opioid receptors modulate ultrasonic vocalization production via a common mechanism. To that end, 11-day-old rats were injected with the α 2-adrenoceptor antagonist yohimbine (0, 0.5, or 1.0 mg/kg, i.p.) or the κ-opioid receptor antagonist nor-binaltorphimine (0, 5, or 10 mg/kg, i.p.). After 15 min, the same rats were injected with saline, the α 2-adrenoceptor agonist clonidine (0.25 mg/kg, i.p.), or the κ-opioid receptor agonist trans-(±)-3,4-dichloro- N-methyl- N-[2-(1-pyrrolidinyl)-cyclohexyl]-benzeneacetamide methanesulfonate (U-50,488; 2.5 mg/kg, i.p.). Results showed that both clonidine and U-50,488 increased the ultrasonic vocalizations of preweanling rats. Not surprisingly, clonidine-induced ultrasonic vocalizations were blocked by yohimbine, while U-50,488-induced vocalizations were blocked by nor-binaltorphimine. Importantly, yohimbine also attenuated the vocalizations produced by U-50,488, whereas nor-binaltorphimine did not alter clonidine-induced ultrasonic vocalizations. Thus, it appears that α 2-adrenoceptor and κ-opioid receptor stimulation increases ultrasonic vocalization production via a common mechanism. It is likely that the κ-opioid receptors responsible for modulating ultrasonic vocalizations are located “upstream” from the α 2-adrenoceptors.