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内源性多巴胺对D-1受体的刺激在突触后D-2介导的行为反应表达中的允许作用。大鼠打哈欠。

Permissive role of D-1 receptor stimulation by endogenous dopamine for the expression of postsynaptic D-2-mediated behavioural responses. Yawning in rats.

作者信息

Longoni R, Spina L, Di Chiara G

出版信息

Eur J Pharmacol. 1987 Feb 10;134(2):163-73. doi: 10.1016/0014-2999(87)90162-2.

Abstract

Low doses of BHT 920, LY 171555 and (+)3PPP, three dopamine agonists selective for D-2 receptors, induced yawning in rats. This effect was reduced by the selective D-1 antagonist SCH 23390 but the antagonism did not exceed a 50% reduction from the control values. In contrast, the selective D-2 antagonist (-)sulpiride completely abolished agonist-induced yawning. A 6 h reserpine pretreatment (5 mg/kg i.p.), which depletes brain dopamine (DA) by about 95%, reduced agonist-induced yawning by an extent similar to SCH 23390; in the reserpinized rats, SCH 23390 completely lost the property of blocking agonist-induced yawning while (-)sulpiride retained it. Two 5HT receptor antagonist, ketanserin and metergoline failed to influence agonist-induced yawning. The reportedly selective D-1 agonist, SKF 38393, failed to induce yawning in normal rats as well as in rats pretreated with reserpine 6 or 16 h earlier. If one excludes that SCH 23390 and the D-2 agonists interact with the same DA-receptors, the data are consistent with the possibility that stimulation of D-1 receptors by endogenous DA plays a permissive-facilitatory role for the behavioural expression of D-2 receptor activation.

摘要

低剂量的BHT 920、LY 171555和(+)3PPP这三种对D-2受体有选择性的多巴胺激动剂可诱导大鼠打哈欠。这种效应被选择性D-1拮抗剂SCH 23390减弱,但拮抗作用并未超过对照值降低50%。相比之下,选择性D-2拮抗剂(-)舒必利完全消除了激动剂诱导的打哈欠。6小时的利血平预处理(腹腔注射5mg/kg)可使脑内多巴胺(DA)减少约95%,其降低激动剂诱导打哈欠的程度与SCH 23390相似;在利血平化的大鼠中,SCH 23390完全失去了阻断激动剂诱导打哈欠的特性,而(-)舒必利仍保留该特性。两种5-羟色胺受体拮抗剂酮色林和麦角林未能影响激动剂诱导的打哈欠。据报道具有选择性的D-1激动剂SKF 38393在正常大鼠以及提前6或16小时用利血平预处理的大鼠中均未能诱导打哈欠。如果排除SCH 23390和D-2激动剂与相同的DA受体相互作用,这些数据与内源性DA刺激D-1受体对D-2受体激活的行为表达起允许促进作用的可能性一致。

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