Background: Rats emit 50-kHz ultrasonic vocalizations (USVs) to communicate positive emotional states, and these USVs are increasingly being investigated in preclinical studies on reward and motivation. Although it is the activation of dopamine receptors that initiates the emission of 50-kHz USVs, non-dopaminergic mechanisms may modulate calling in the 50 kHz frequency band. To further elucidate these mechanisms, the present study investigated whether the pharmacological manipulation of glucocorticoid signaling influenced calling. Methods: Rats were administered corticosterone (1-5 mg/kg, s.c.), the glucocorticoid receptor antagonist mifepristone (40 or 100 mg/kg, s.c.), or the corticosterone synthesis inhibitor metyrapone (50 or 100 mg/kg, i.p.). The effects of these drugs on calling initiation and on calling recorded during nonaggressive social contacts or after the administration of amphetamine (0.25 or 1 mg/kg, i.p.) were then evaluated. Results: Corticosterone failed to initiate the emission of 50-kHz USVs and did not influence pro-social and amphetaminestimulated calling. Similarly, mifepristone and metyrapone did not initiate calling. However, metyrapone suppressed prosocial calling and calling stimulated by a moderate dose (1 mg/kg, i.p.) of amphetamine. Conversely, mifepristone attenuated calling stimulated by a low (0.25 mg/kg, i.p.), but not moderate (1 mg/kg, i.p.), dose of amphetamine and had no influence on pro-social calling. Conclusions: The present results demonstrate that glucocorticoid signaling modulates calling in the 50 kHz frequency band only in certain conditions and suggest that mechanisms different from the inhibition of corticosterone synthesis mayparticipate in the suppression of calling by metyrapone.
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