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首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Noradrenergic mechanism involved in the nociceptive modulation of hippocampal CA3 region of normal rats
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Noradrenergic mechanism involved in the nociceptive modulation of hippocampal CA3 region of normal rats

机译:去甲肾上腺素能机制参与正常大鼠海马CA3区的伤害性调节

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摘要

Norepinephrine (NE) is an important neurotransmitter in the brain, and regulates antinociception. However, the mechanism of action of NE on pain-related neurons in the hippocampal CA3 region is not clear. This study examines the effects of NE, phentolamine on the electrical activities of pain-excited neurons (PENs) and pain-inhibited neurons (PINs) in the hippocampal CA3 region of rats. Trains of electric impulses applied to the right sciatic nerve were used as noxious stimulation. The electrical activities of PENs or PINs in the hippocampal CA3 region were recorded by using a glass microelectrode. Our results revealed that, in the hippocampal CA3 region, the intra-CA3 region microinjection of NE decreased the pain-evoked discharged frequency and prolonged the discharged latency of PEN, and increased the pain-evoked discharged frequency and shortened discharged inhibitory duration (ID) of PIN, exhibiting the specific analgesic effect of NE. While intra-CA3 region microinjection of phentolamine produced the opposite response. It implies that phentolamine can block the effect of endogenous NE to cause the enhanced response of PEN and PIN to noxious stimulation. On the basis of above findings we can deduce that NE, phentolamine and alpha-adrenoceptor are involved in the modulation of nociceptive information transmission in the hippocampal CA3 region.
机译:去甲肾上腺素(NE)是大脑中重要的神经递质,调节抗伤害感受。但是,NE对海马CA3区疼痛相关神经元的作用机制尚不清楚。这项研究检查了NE,酚妥拉明对大鼠海马CA3区疼痛刺激神经元(PEN)和疼痛抑制神经元(PIN)电活动的影响。施加于右坐骨神经的电脉冲序列被用作有害刺激。使用玻璃微电极记录海马CA3区PEN或PIN的电活动。我们的研究结果表明,在海马CA3区中,NE的CA3区内显微注射降低了疼痛诱发的放电频率并延长了PEN的放电潜伏期,增加了疼痛诱发的放电频率并缩短了放电抑制持续时间(ID) PIN,具有NE的特定镇痛作用。虽然在CA3区域内注射酚妥拉明产生了相反的反应。这表明酚妥拉明可以阻断内源性NE的作用,引起PEN和PIN对有害刺激的增强反应。根据以上发现,我们可以推断出NE,酚妥拉明和α-肾上腺素能受体参与了海马CA3区伤害性信息传递的调节。

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