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首页> 外文期刊>Brazilian Journal of Medical and Biological Research >Antinociception induced by stimulating amygdaloid nuclei in rats: changes produced by systemically administered antagonists
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Antinociception induced by stimulating amygdaloid nuclei in rats: changes produced by systemically administered antagonists

机译:刺激大鼠杏仁核诱导的镇痛作用:全身性拮抗剂产生的变化

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摘要

The antinociceptive effects of stimulating the medial (ME) and central (CE) nuclei of the amygdala in rats were evaluated by the changes in the latency for the tail withdrawal reflex to noxious heating of the skin. A 30-s period of sine-wave stimulation of the ME or CE produced a significant and short increase in the duration of tail flick latency. A 15-s period of stimulation was ineffective. Repeated stimulation of these nuclei at 48-h intervals produced progressively smaller effects. The antinociception evoked from the ME was significantly reduced by the previous systemic administration of naloxone, methysergide, atropine, phenoxybenzamine, and propranolol, but not by mecamylamine, all given at the dose of 1.0 mg/kg. Previous systemic administration of naloxone, atropine, and propranolol, but not methysergide, phenoxybenzamine, or mecamylamine, was effective against the effects of stimulating the CE. We conclude that the antinociceptive effects of stimulating the ME involve at least opioid, serotonergic, adrenergic, and muscarinic cholinergic descending mechanisms. The effects of stimulating the CE involve at least opioid, ?-adrenergic, and muscarinic cholinergic descending mechanisms.
机译:刺激大鼠杏仁核中枢(ME)和中央(CE)核的镇痛作用通过改变尾巴反射对皮肤有害加热的潜伏时间来评估。 ME或CE的30秒正弦波刺激会导致甩尾潜伏期的持续时间显着而短暂地增加。 15秒的刺激时间无效。以48小时的间隔重复刺激这些核产生的作用逐渐减小。先前全身性给予纳洛酮,美塞麦肽,阿托品,苯氧基苯甲胺和普萘洛尔的全身性给药显着降低了由ME引起的抗伤害感受,但美卡明胺均没有,均以1.0 mg / kg的剂量给予。先前对纳洛酮,阿托品和普萘洛尔进行全身性给药,但对美塞麦肽,苯氧基苯甲胺或美卡明胺无效,对刺激CE效果有效。我们得出结论,刺激ME的抗伤害感受作用至少涉及阿片样物质,血清素能,肾上腺素能和毒蕈碱型胆碱能下降机制。刺激CE的作用至少涉及阿片样物质,β-肾上腺素能和毒蕈碱型胆碱能下降机制。

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