Dopamine D3 receptor knock-out mice display deficits in locomotor sensitization after chronic morphine administration
Dopamine D3 receptor knock-out mice display deficits in locomotor sensitization after chronic morphine administration
复制标题
多巴胺 D3 受体敲除小鼠在长期服用吗啡后表现出运动敏化缺陷
DOI:
10.1016/j.neulet.2010.09.025
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发表时间:
2010-11-26
影响因子:
2.5
通讯作者:
Li, Sheng-bing
中科院分区:
文献类型:
--
作者:
Li, Tao;Hou, Ying;Li, Sheng-bing
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 2 mg/kg naloxone was co-administered with 10 mg/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. (C) 2010 Elsevier Ireland Ltd. All rights reserved.