SELECTIVE ANTAGONISM OF DOPAMINE D-1 AND D-2 RECEPTORS DOES NOT BLOCK THE DEVELOPMENT OF BEHAVIORAL SENSITIZATION TO COCAINE
SELECTIVE ANTAGONISM OF DOPAMINE D-1 AND D-2 RECEPTORS DOES NOT BLOCK THE DEVELOPMENT OF BEHAVIORAL SENSITIZATION TO COCAINE
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DOI：
10.1007/bf02244843
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发表时间：
1994-03-01
影响因子：
3.4
通讯作者：
PERKINS, C
中科院分区：
文献类型：
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作者：
MATTINGLY, BA;HART, TC;PERKINS, C
本研究的目的是确定D-1或D-2选择性多巴胺受体拮抗剂是否可以阻止对可卡因行为致敏的发展。雄性Wistar大鼠每天用可卡因（15 mg/kg， IF）或对照剂联合D-1多巴胺拮抗剂SCH 23390 （0.3 mg/kg， SC）、D-2多巴胺拮抗剂舒比利（100 mg/kg， IF）或对照剂治疗7天。每日注射后，测定大鼠光电池竞技场的运动活性。在最后一次暴露前试验24小时后，所有大鼠均给予可卡因（15 mg/kg， IF）攻毒注射并检测活动。可卡因治疗在重复暴露（即致敏）时产生了更大的运动活动相对增加。此外，sch23390和舒必利都能减弱可卡因引起的运动活动的增加。相比之下，舒必利和SCH 23390都不能阻断对可卡因行为致敏的发展。也就是说，用舒必利或SCH 23390和可卡因预处理的大鼠与只预先暴露于可卡因的大鼠在给予可卡因刺激注射时没有区别。这些结果表明，对可卡因的行为致敏可能通过刺激D-1或D-2多巴胺受体产生，也可能通过刺激某些非多巴胺能受体产生。
The objective of this study was to determine whether the development of behavioral sensitization to cocaine could be prevented by either D-1 or D-2 selective dopamine receptor antagonists. Male Wistar rats were treated daily for 7 days with either cocaine (15 mg/kg, IF) or vehicle in combination with the D-1 dopamine antagonist SCH 23390 (0.3 mg/kg, SC), the D-2 dopamine antagonist sulpiride (100 mg/kg, IF), or vehicle. After the daily injections, the rats were tested for locomotor activity in photocell arenas. Twenty-four hours after the last pre-exposure test session, all rats were given a challenge injection of cocaine (15 mg/kg, IF) and tested for activity. Cocaine treatments produced a greater relative increase in locomotor activity with repeated exposure (i.e. sensitization). Moreover, this increase in cocaine-induced locomotor activity was attenuated by both SCH 23390 and sulpiride. In contrast, neither sulpiride nor SCH 23390 blocked the development of behavioral sensitization to cocaine. That is, rats pretreated with sulpiride or SCH 23390 and cocaine did not differ from rats pre-exposed only to cocaine when given a cocaine challenge injection. These results suggest that behavioral sensitization to cocaine may develop through either D-1 or D-2 dopamine receptor stimulation or possibly through stimulation of some non-dopaminergic receptor.