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学科主题: 药物依赖
题名:
Buspirone-induced antinociception is mediated by L-type calcium channels and calcium/caffeine-sensitive pools in mice
作者: Liang, JH; Wang, XH; Liu, RK; Sun, HL; Ye, XF; Zheng, JW
关键词: buspirone ; fluoxetine ; calcium channel blocker ; ryanodine ; nociception ; the hot-plate test
刊名: PSYCHOPHARMACOLOGY
发表日期: 2003-03-01
DOI: 10.1007/s00213-002-1327-4
卷: 166, 期:3, 页:276-283
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Neurosciences ; Pharmacology & Pharmacy ; Psychiatry
研究领域[WOS]: Neurosciences & Neurology ; Pharmacology & Pharmacy ; Psychiatry
关键词[WOS]: RAT SPINAL-CORD ; N-TYPE ; DIVALENT-CATIONS ; 5-HT1A RECEPTORS ; CHOLINERGIC ANTINOCICEPTION ; SEROTONERGIC INHIBITION ; MORPHINE ANALGESIA ; SENSORY NEURONS ; XENOPUS LARVAE ; RAPHE NEURONS
英文摘要:

Rationale: Previous studies have shown that buspirone, a partial 5-HT1A receptor agonist, produces antinociceptive effects in rats and mice; Ca2+ plays a critical role as a second messenger in mediating nociceptive transmission. 5-HT1A receptors have been proven to be coupled functionally with various types of Ca2+ channels in neurons, including N-, P/Q-, T-, or L-type. It was of interest to investigate the involvement of extracellular/intracellular Ca2+ in buspirone-induced antinociception. Objectives: To determine whether central serotonergic pathways participate in the antinociceptive processes of buspirone, and investigate the involvement of Ca2+ mechanisms, particularly L-voltage-gated Ca2+ channels and Ca2+/caffeine-sensitive pools, in buspironeinduced antinociception. Methods: Antinociception was assessed using the hot-plate test (55degreesC, hind-paw licking latency) in mice treated with either buspirone (1.25-20 mg/kg i.p.) alone or the combination of buspirone and fluoxetine (2.5-10 mg/kg i.p.), 5-HTP (25 mg/kg i.p.), nimodipine (2.5-10 mg/kg i.p.), nifedipine (2.5-10 mg/kg i.p.), CaCl2 (25-200 nmol per mouse i.c.v.), EGTA (530 nmol per mouse i.c.v.), or ryanodine (0.25-2 nmol per mouse i.c.v.). Results: Buspirone dose dependently increased the licking latency in the hot-plate test in mice. This effect of buspirone was enhanced by fluoxetine, 5-HTP, nimodipine, and nifedipine. Interestingly, central administration of Ca2+ reversed the antinociceptive effects of buspirone. In contrast to these, ryanodine or EGTA administered centrally potentiated buspirone-induced antinociception. Conclusions Decreasing neuronal Ca2+ levels potentiated buspirone-induced antinociception; conversely, increasing intracellular Ca2+ abolished the antinociceptive effects of buspirone. These results suggest that Ca2+ influx from extracellular fluid and release of Ca2+ from Ca2+/caffeine- sensitive microsomal pools may be involved in buspirone-induced antinociception.

语种: 英语
WOS记录号: WOS:000182202000012
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/50505
Appears in Collections:中国药物依赖性研究所_期刊论文

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作者单位: Peking Univ, Natl Inst Drug Dependence, Dept Neuropharmacol, Beijing 100083, Peoples R China

Recommended Citation:
Liang, JH,Wang, XH,Liu, RK,et al. Buspirone-induced antinociception is mediated by L-type calcium channels and calcium/caffeine-sensitive pools in mice[J]. PSYCHOPHARMACOLOGY,2003,166(3):276-283.
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