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5-羟色胺能抑制对大鼠中多巴胺受体激动剂诱发呵欠的增强作用。

Potentiation by serotonergic inhibition of yawning induced by dopamine receptor agonists in rats.

作者信息

Matsumoto S, Yamada K, Nagashima M, Matsuo N, Shirakawa K, Furukawa T

机构信息

Department of Pharmacology, School of Medicine, Fukuoka University, Japan.

出版信息

Pharmacol Biochem Behav. 1989 Mar;32(3):815-8. doi: 10.1016/0091-3057(89)90039-7.

Abstract

Low doses of the dopamine D2-receptor agonist, B-HT 920 (25 micrograms/kg, SC), and the dopamine D1/D2-receptor agonists, apomorphine (50 micrograms/kg, SC) and piribedil (1 mg/kg, SC), evoked yawning. However, the dopamine D1-receptor agonist, SK&F 38393 (2 mg/kg, SC), failed to induce yawning. The yawning responses induced by B-HT 920, apomorphine or piribedil were markedly increased without eliciting stereotypy by pretreatment with reserpine (5 mg/kg, IP, 24 hr). These yawning responses were also enhanced by p-chlorophenylalanine (PCPA) (300 mg/kg, IP, 72 hr), but not by alpha-methyl-p-tyrosine (300 mg/kg, IP, 6 hr). The yawning induced by B-HT 920 given alone and in combination with reserpine or PCPA was inhibited by spiperone (0.5 mg/kg, IP) or scopolamine (0.5 mg/kg, IP), but not by SCH 23390 (0.5 mg/kg, IP). The present results suggest that yawning is evoked by stimulation of dopamine D2-receptors having a high affinity and consequent muscarinic activation, and that the yawning induced by dopamine receptor agonists is potentiated by decreases in serotonergic neuron activity.

摘要

低剂量的多巴胺D2受体激动剂B-HT 920(25微克/千克,皮下注射)、多巴胺D1/D2受体激动剂阿扑吗啡(50微克/千克,皮下注射)和匹立哌唑(1毫克/千克,皮下注射)可诱发打哈欠。然而,多巴胺D1受体激动剂SK&F 38393(2毫克/千克,皮下注射)未能诱发打哈欠。用利血平(5毫克/千克,腹腔注射,24小时)预处理后,B-HT 920、阿扑吗啡或匹立哌唑诱导的打哈欠反应显著增强,且未引发刻板行为。对氯苯丙氨酸(PCPA)(300毫克/千克,腹腔注射,72小时)也可增强这些打哈欠反应,但α-甲基对酪氨酸(300毫克/千克,腹腔注射,6小时)则无此作用。单独给予B-HT 920以及与利血平或PCPA联合给予时所诱导的打哈欠,可被螺哌隆(0.5毫克/千克,腹腔注射)或东莨菪碱(0.5毫克/千克,腹腔注射)抑制,但不受SCH 23390(0.5毫克/千克,腹腔注射)抑制。目前的结果表明,高亲和力多巴胺D2受体的刺激及随之而来的毒蕈碱激活可诱发打哈欠,且多巴胺受体激动剂诱导的打哈欠会因血清素能神经元活动的降低而增强。

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