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Role of central melanotropinergic and adrenergic neurons in neuronal mechanisms involved in yawning behavior.

中枢促黑素能和肾上腺素能神经元在涉及打哈欠行为的神经元机制中的作用。

基本信息

批准号：
62570098
负责人：
YAMADA Katsushi
金额：
$ 1.15万
依托单位：
Fukuoka University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1987
资助国家：
日本
起止时间：
1987 至 1988
项目状态：
已结题

项目摘要

The present experiments were performed to understand the role of central adrenergic and melanotropinergic neurons in neuronal mechanisms involved in yawning behavior in rats. Yawning was evoked by subcutaneous injections of apomorphine and piribedil, mixed dopamine D_1/D_2-receptor agonists, but not by SK＆F 38393, a dopamine D_1-receptor agonist. The putative dopamine autoreceptor agonists, talipexole and snd 919 also elicited yawning. The yawning induced by these dopamine receptor agonists was increased by pindolol and propranolol which block the central beta-adrenoceptors, but not by the peripheral beta-adrenoceptor antagonists, carteolol and atenolol. these beta-adrenoceptor antagonists given alone did not elicit yawning. Conversely, the yawning was inhibited by salbutamol, a beta-adrenoceptor agonist, without being affected by prazosin, an alpha-adrenoceptor antagonist. The combined administration of SK＆F 38393 and the beta-adrenoceptor antagonists did not induce yawning.The yawnin … More g elicited by either apomorphine or piribedil in combination with pindolol was suppressed by spiperone and YM-09151-2, dopamine D_2-receptor antagonists, and scopolamine, a muscarinic receptor antagonist, but not by SCH 23390, a dopamine D_1-receptor antagonist. Physostigmine or pilocarpine induced yawning, which was also enhanced by pindolol and propranolol. This enhanced yawning was inhibited by scopolamine, but not by spiperone, YM-09151-2 and SCH 23390. On the other hand, the yawning responses induced by talipexole, apomorphine or piribedil were markedly increased without eliciting stereotypy by reserpine and p-chlorophenylalanine. Furthermore, yawning was observed after low doses of talipexole or SND 919, but was not observed after very high doses of the drugs. The high doses of talipexole or SND 919 given alone evoked a slight stereotypy, which was enhanced by the combined treatment with SK＆F 38393. However, low and effective doses for inducing yawning of talipexole or SND 919 in combination with SK＆F 38393 did not elicit stereotypy. The present results suggest that yawning is evoked by stimulation of dopamine D_2-receptors having a high affinity and consequent muscarinic activation, and that the beta-adrenoceptor blockade facilitates the occurrence of yawning induced by dopaminergic and cholinergic agonists. It was also suggested that the yawning induced by dopamine receptor agonists is potentiated by decreases in serotonergic neuron activity and that the stereotypy-related dopamine D_2-receptors not only cooperate with the dopamine D_1-receptors but also be less sensitive than the yawning-related dopamine D_2-receptors. Less

本实验旨在了解中枢肾上腺素能和促黑素能神经元在大鼠打哈欠行为神经机制中的作用。皮下注射多巴胺D_1/D_2受体激动剂阿扑吗啡和吡贝地尔可诱发打哈欠，而多巴胺D_1受体激动剂SK& F38393则不能诱发打哈欠。多巴胺自身受体激动剂talipexole和snd 919也能引起打哈欠。这些多巴胺受体激动剂引起的哈欠增加吲哚洛尔和普萘洛尔，阻断中央β-肾上腺素受体，但不是由外周β-肾上腺素受体拮抗剂，卡替洛尔和阿替洛尔。单独给予这些β-肾上腺素受体拮抗剂不会引起打哈欠。相反，沙丁胺醇，β-肾上腺素能受体激动剂，抑制打哈欠，而不受哌唑嗪，α-肾上腺素能受体拮抗剂。SK&F 38393和β-肾上腺素受体拮抗剂的联合给药不诱导打哈欠。 ...更多信息多巴胺D_2受体拮抗剂Spiperone、YM-09151-2和M受体拮抗剂东莨菪碱均能抑制阿扑吗啡或吡贝地尔与吲哚洛尔合用所引起的g，而多巴胺D_1受体拮抗剂SCH 23390则不抑制。毒扁豆碱或毛果芸香碱引起打哈欠，吲哚洛尔和普萘洛尔也能增强这种作用。东莨菪碱可抑制这种增强的打哈欠，但螺哌隆、YM-09151-2和SCH 23390不能抑制。另一方面，由他立泊索、阿扑吗啡或吡贝地尔引起的哈欠反应显著增加，而利血平和对氯苯丙氨酸不引起刻板反应。此外，在低剂量的他立普索或SND 919后观察到打哈欠，但在非常高剂量的药物后未观察到打哈欠。单独给予高剂量的他立泊索或SND 919引起轻微的刻板印象，这通过与SK&F 38393的组合治疗而增强。然而，低剂量和有效剂量的他立泊索或SND 919与SK&F 38393的组合诱导打哈欠不会引起刻板症。本实验结果提示，打哈欠是由高亲和力的多巴胺D_2受体的刺激和随后的毒蕈碱激活引起的，阻断β-肾上腺素受体可促进多巴胺能和胆碱能激动剂引起的打哈欠的发生。多巴胺能神经元活动的减少可增强多巴胺受体激动剂诱发的哈欠;刻板印象相关多巴胺D_2受体不仅与多巴胺D_1受体协同作用，而且不如哈欠相关多巴胺D_2受体敏感。少