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胆碱能机制参与齿状回的伤害性调制。

Cholinergic mechanism involved in the nociceptive modulation of dentate gyrus.

作者信息

Jiao Runsheng, Yang Chunxiao, Zhang Ying, Xu Manying, Yang Xiaofang

机构信息

Department of Physiology, Harbin Medical University, XueFu Road No. 194, NanGang District, Harbin 150081, Heilongjiang Province, PR China.

出版信息

Biochem Biophys Res Commun. 2009 Feb 20;379(4):975-9. doi: 10.1016/j.bbrc.2008.12.184. Epub 2009 Jan 9.

Abstract

Acetylcholine (ACh) causes a wide variety of anti-nociceptive effects. The dentate gyrus (DG) region of the hippocampal formation (HF) has been demonstrated to be involved in nociceptive perception. However, the mechanisms underlying this anti-nociceptive role have not yet been elucidated in the cholinergic pain-related neurons of DG. The electrical activities of pain-related neurons of DG were recorded by a glass microelectrode. Two kinds of pain-related neurons were found: pain-excited neurons (PEN) and pain-inhibited neurons (PIN). The experimental protocol involved intra-DG administration of muscarinic cholinergic receptor (mAChR) agonist or antagonist. Intra-DG microinjection of 1 microl of ACh (0.2 microg/microl) or 1 microl of pilocarpine (0.4 microg/microl) decreased the discharge frequency of PEN and prolonged firing latency, but increased the discharge frequency of PIN and shortened PIN inhibitory duration (ID). Intra-DG administration of 1 microl of atropine (1.0 microg/microl) showed exactly the opposite effects. According to the above experimental results, we can presume that cholinergic pain-related neurons in DG are involved in the modulation of the nociceptive response by affecting the discharge of PEN and PIN.

摘要

乙酰胆碱(ACh)具有多种抗伤害感受作用。海马结构(HF)的齿状回(DG)区域已被证明与伤害感受知觉有关。然而,DG中胆碱能疼痛相关神经元的这种抗伤害感受作用的潜在机制尚未阐明。用玻璃微电极记录DG中疼痛相关神经元的电活动。发现了两种疼痛相关神经元:疼痛兴奋神经元(PEN)和疼痛抑制神经元(PIN)。实验方案包括在DG内给予毒蕈碱胆碱能受体(mAChR)激动剂或拮抗剂。在DG内微量注射1微升ACh(0.2微克/微升)或1微升毛果芸香碱(0.4微克/微升)可降低PEN的放电频率并延长放电潜伏期,但增加PIN的放电频率并缩短PIN的抑制持续时间(ID)。在DG内给予1微升阿托品(1.0微克/微升)则表现出完全相反的效果。根据上述实验结果,我们可以推测DG中的胆碱能疼痛相关神经元通过影响PEN和PIN的放电参与伤害性反应的调节。

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