Characterization of the dopamine D3 receptor agonist R(+)-7-hydroxy-N, N-di-n-propyl-2-aminotetralin-induced hypo- and hypermotility in mice

✍ Scribed by Makoto Ukai; Hiroko Tamoto; Tomoko Tanaka; Tsutomu Kameyama

• Publisher: John Wiley and Sons
• Year: 1999
• Tongue: English
• Weight: 121 KB
• Volume: 14
• Category: Article
• ISSN: 0885-6222
• DOI: 10.1002/(sici)1099-1077(199910)14:7<453::aid-hup126>3.0.co;2-o

✦ Synopsis

The present study was designed to characterize the dopamine D 3 receptor agonist R()-7-hydroxy-N,N-di-n-propyl-2-aminotetralin (R()-7-OH-DPAT)-induced changes in locomotor activity in mice. Although R()-7-OH-DPAT (0 . 01±10 mg/kg) produced a signi®cant decrease in horizontal and vertical motility within 15 min after the start of behavioural measurements, the dopamine D 1 receptor antagonist R()-SCH23390 (0 . 05 mg/kg) and the dopamine D 3 receptor antagonist ()-UH232 (10 mg/kg) had no antagonistic eects on the R()-7-OH-DPAT (3 mg/kg)induced hypomotility, while the dopamine D 2 receptor antagonist S(À)-sulpiride (20 mg/kg) augmented it. Although R()-7-OH-DPAT (0 . 01±1 mg/kg) had no marked eects on horizontal or vertical motility, higher doses (3 and 10 mg/kg) of the drug produced a signi®cant increase in horizontal or vertical motility from 30 to 90 min after the start of the behavioural measurements. S(À)-sulpiride (20 mg/kg) and ()-UH232 (10 mg/kg) almost completely inhibited the R()-7-OH-DPAT (3 mg/kg)-induced hypermotility, whereas the antagonistic eects of R()-SCH23390 (0 . 05 mg/kg) were partial. These results suggest that the R()-7-OH-DPAT-induced hypermotility is mediated principally via dopamine D 2 and D 3 receptors, whereas it is unlikely that the hypomotility results from the activation of presynaptic dopamine D 2 or D 3 receptors.