Dias Flávia Regina Cruz, Carey Robert J, Carrera Marinete Pinheiro
Behavioral Pharmacology Group, Laboratory of Animal Health, State University of North Fluminense, Avenida Alberto Lamego 2000, Campos dos Goytacazes, 28013-600 RJ, Brazil.
Brain Res. 2006 Apr 14;1083(1):85-95. doi: 10.1016/j.brainres.2006.02.002. Epub 2006 Mar 10.
The present study examined the role of D(1) and D(2) receptors in the conditioning of apomorphine-induced locomotor behavior. A Pavlovian conditioning protocol was used in which rats received 5 daily intrastriatal apomorphine treatments paired or unpaired to an open-field environment followed, 2 days later, by a saline test for conditioning. In the conditioning induction phase, the intrastriatal apomorphine treatment increased locomotor activity expressed as an increased number of sectional crossings and rearings. In the conditioning test, the apomorphine-paired group had significantly higher locomotor activity than the unpaired and vehicle groups, consistent with the development of a conditioned locomotor response. The concomitant blockade of D(1) and D(2) receptors with D(1) (SCH23390) and D(2) (sulpiride) antagonists prevented the apomorphine-induced behavioral response during the induction phase and in the conditioning test. Pretreatment with the D(1) antagonist SCH 23390 also blocked the apomorphine-induced behavioral response during the induction phase but did not block the apomorphine conditioned response. Pretreatment with the selective D(2) antagonist sulpiride blocked the apomorphine behavioral response during the induction phase and in the conditioning test. Altogether, these results indicate that antagonism of either the D(1) or D(2) receptors in the dorsal striatum can block apomorphine-induced locomotor activation but that D(2) but not D(1) antagonism can prevent the development of the apomorphine conditioned response. Altogether, these findings indicate a key role for the D(2) receptor site in the mediation of apomorphine conditioned behavior; and, in addition, that apomorphine conditioned locomotor response can develop without the expression of the locomotor stimulant response during the induction phase of conditioning.
本研究考察了D(1)和D(2)受体在阿扑吗啡诱导的运动行为条件反射中的作用。采用了经典条件反射实验方案,即大鼠每天接受5次纹状体内注射阿扑吗啡,注射与旷场环境配对或不配对,2天后进行生理盐水条件反射测试。在条件反射诱导阶段,纹状体内注射阿扑吗啡可增加运动活性,表现为穿越分区次数和直立次数增加。在条件反射测试中,阿扑吗啡配对组的运动活性显著高于未配对组和溶剂对照组,这与条件性运动反应的形成一致。同时使用D(1)受体拮抗剂SCH23390和D(2)受体拮抗剂舒必利阻断D(1)和D(2)受体,可在诱导阶段和条件反射测试中阻止阿扑吗啡诱导的行为反应。预先使用D(1)受体拮抗剂SCH23390也可在诱导阶段阻断阿扑吗啡诱导的行为反应,但不能阻断阿扑吗啡条件反应。预先使用选择性D(2)受体拮抗剂舒必利可在诱导阶段和条件反射测试中阻断阿扑吗啡的行为反应。总之,这些结果表明,阻断背侧纹状体中的D(1)或D(2)受体均可阻断阿扑吗啡诱导的运动激活,但只有阻断D(2)受体而非D(1)受体才能阻止阿扑吗啡条件反应的形成。总之,这些发现表明D(2)受体位点在介导阿扑吗啡条件行为中起关键作用;此外,阿扑吗啡条件性运动反应可在条件反射诱导阶段不出现运动兴奋反应的情况下形成。