title: Inhibition of 50-kHz ultrasonic vocalizations by dopamine receptor subtype-selective agonists and antagonists in adult rats.
abstract: BACKGROUND
  Adult rats emit ultrasonic calls at around 22 and 50 kHz, which are often elicited by aversive and rewarding stimuli, respectively. Dopamine (DA) plays a role in aspects of both reward and aversion.
  
  
  OBJECTIVE
  The purpose of this study is to investigate the effects of DA receptor subtype-selective agonists on 22- and 50-kHz call rates.
  
  
  METHODS
  Ultrasonic calls were recorded in adult male rats that were initially screened with amphetamine to eliminate low 50-kHz callers. The remaining subjects were tested after acute intraperitoneal or subcutaneous injection of the following DA receptor-selective agonists and antagonists: A68930 (D1-like agonist), quinpirole (D2-like agonist), PD 128907 (D3 agonist), PD 168077 (D4 agonist), SCH 39166 (D1-like antagonist), L-741,626 (D2 antagonist), NGB 2904 (D3 antagonist), and L-745,870 (D4 antagonist). The indirect DA/noradrenaline agonist amphetamine served as a positive control.
  
  
  RESULTS
  As expected, amphetamine strongly increased 50-kHz call rates. In contrast, D1-, D2-, and D3-selective DA receptor agonists, when given alone, inhibited calling; combinations of D1- and D2-like agonists also decreased call rate. Given alone, the D1-like and D3 antagonists significantly decreased call rate, with a similar trend for the D2 antagonist. Agonist-antagonist combinations also decreased calling. The D4 agonist and antagonist did not significantly affect 50-kHz call rates. Twenty-two-kilohertz calls occurred infrequently under all drug conditions.
  
  
  CONCLUSIONS
  Following systemic drug administration, tonic pharmacological activation of D1-like or D2-like DA receptors, either alone or in combination, does not appear sufficient to induce 50-kHz calls. Dopaminergic transmission through D1, D2, and D3 receptors appears necessary for spontaneous calling.
authors.affiliation: Department of Pharmacology and Therapeutics, McGill University, McIntyre Medical Building Rm. 1320, 3655 Promenade Sir William Osler, Montreal, QC, H3G 1Y6, Canada.
authors.forename: Tina
authors.initials: T
authors.lastname: Scardochio
authors.forename: Paul B S
authors.initials: PB
authors.lastname: Clarke
mesh_terms: D000661:Amphetamine / Q000494:pharmacology; D000818:Animals; D004298:Dopamine / Q000378:metabolism*; D018491:Dopamine Agonists / Q000494:pharmacology; D018492:Dopamine Antagonists / Q000494:pharmacology; D065127:Dopamine D2 Receptor Antagonists; D008297:Male; D051381:Rats; D020318:Rats, Long-Evans; D017447:Receptors, Dopamine D1 / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism*; D017448:Receptors, Dopamine D2 / Q000819:agonists / Q000378:metabolism*; D050637:Receptors, Dopamine D3 / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism*; D012201:Reward; D014465:Ultrasonics; D014828:Vocalization, Animal / Q000187:drug effects
chemical_list: D018491:Dopamine Agonists; D018492:Dopamine Antagonists; D065127:Dopamine D2 Receptor Antagonists; D017447:Receptors, Dopamine D1; D017448:Receptors, Dopamine D2; D050637:Receptors, Dopamine D3; D000661:Amphetamine; D004298:Dopamine