Szumlinski Karen K, Szechtman Henry
Department of Psychiatry and Behavioural Neurosciences, McMaster University, 1200 Main St. West, Hamilton, Ontario, Canada L8N 3Z5.
Neuroreport. 2002 Apr 16;13(5):563-6. doi: 10.1097/00001756-200204160-00005.
The D2/D3 dopamine receptor agonist quinpirole (QNP) produces biphasic effects on locomotion and can induce oral behaviour. To determine whether or not these behaviours result from actions of QNP at D2 receptors located in the dorsal raphe, nucleus (DRN), rats were pretreated intra-DRN with the selective dopamine D2 receptor antagonist, raclopride (0, 1 or 2 microg) prior to an acute peripheral injection of QNP (0 or 0.5 mg/kg, s.c.). Intra-DRN raclopride did not affect QNP-induced oral activity or QNP-induced locomotor inhibition. However, the high dose of raclopride potentiated QNP-induced locomotor excitation. These data suggest that D2 receptor activation in the DRN suppresses QNP-induced locomotor excitation, an effect that may be related to D2 receptor-mediated alterations in serotonin transmission.
D2/D3多巴胺受体激动剂喹吡罗(QNP)对运动产生双相效应,并可诱发口腔行为。为了确定这些行为是否源于QNP作用于位于中缝背核(DRN)的D2受体,在急性外周注射QNP(0或0.5mg/kg,皮下注射)之前,给大鼠脑室内注射选择性多巴胺D2受体拮抗剂雷氯必利(0、1或2μg)进行预处理。脑室内注射雷氯必利不影响QNP诱导的口腔活动或QNP诱导的运动抑制。然而,高剂量的雷氯必利增强了QNP诱导的运动兴奋。这些数据表明,DRN中的D2受体激活可抑制QNP诱导的运动兴奋,这种效应可能与D2受体介导的5-羟色胺传递改变有关。