| First Author | Li T | Year | 2010 |
| Journal | Neurosci Lett | Volume | 485 |
| Issue | 3 | Pages | 256-60 |
| PubMed ID | 20849922 | Mgi Jnum | J:167251 |
| Mgi Id | MGI:4867607 | Doi | 10.1016/j.neulet.2010.09.025 |
| Citation | Li T, et al. (2010) Dopamine D3 receptor knock-out mice display deficits in locomotor sensitization after chronic morphine administration. Neurosci Lett 485(3):256-60 |
| abstractText | Locomotor sensitization is the progressive and enduring enhancement of locomotion induced by stimulants such as drugs, which alter rodent locomotion in a long-standing manner. The dopamine D3 receptor has been reported to play a role in morphine addiction. The aim of the present study was to investigate the role of dopamine D3 receptor in the morphine induced locomotor sensitization using dopamine D3 receptor knock-out mice. The dopamine D3 receptor knock-out mice did not display an enhanced behavioral response to acute morphine administration or develop an increased rate of locomotor sensitization to intermittent morphine administration. When 2mg/kg naloxone was co-administered with 10mg/kg morphine, morphine-induced locomotion sensitization in wild-type mice was significantly blocked while the locomotion in the D3 receptor knock-out mice was decreased. Then the wild-type mice were administered with dopamine D3 antagonist nafadotride. It was found that co-administration of morphine with nafadotride could effectively suppress the level of morphine induced behavioral sensitization. It was concluded that a loss of the dopamine D3 receptor gene may inhibit acute morphine induced hyperlocomotor activity and chronic morphine induced behavioral sensitization. |
