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首页> 外文期刊>Brain research bulletin >The antinociceptive effect of anterior pretectal nucleus stimulation is mediated by distinct neurotransmitter mechanisms in descending pain pathways
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The antinociceptive effect of anterior pretectal nucleus stimulation is mediated by distinct neurotransmitter mechanisms in descending pain pathways

机译：前防改造核刺激的抗闭合效应是通过下降疼痛途径中的不同神经递质机制介导的

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摘要

Electrical stimulation of the anterior pretectal nucleus (APtN) activates two descending pain inhibitory pathways. One of these pathways relays in the ipsilateral lateral paragigantocellular nucleus (LPGi), whereas the other pathway relays in the contralateral pedunculopontine tegmental nucleus (PPTg). Antinociceptive effect of APtN stimulation has been seen in various pain models in the rodents. Similarly, LPGi or PPTg stimulation results in higher pain thresholds. Descending antinociceptive pathways activated by electrical APtN stimulation have been elucidated, but the underlying neurotransmitter mechanisms involved have not been clarified yet. This study investigates the role that endogenous signaling plays in the ipsilateral LPGi or contralateral PPTg after the APtN is stimulated in the tail-flick test. First, we submitted rats to excitotoxic injection of N-methyl-D-aspartate (NMDA) into the contralateral PPTg. Then, we examined whether blockage of NMDA (AP-7), serotonergic (methysergide), or opioid (naloxone) receptors in the ipsilateral LPGi is required for APtN stimulation-evoked analgesia (SEA). Likewise, we examined the effects of antagonists of NMDA, serotonergic, or cholinergic nicotinic (mecamylamine) receptors on the contralateral PPTg in ipsilateral LPGi-lesioned rats. Our results confirmed that APtN stimulation activates two pain inhibitory pathways and showed that endogenous opioid signaling in the ipsilateral LPGi appears to be necessary for APtN SEA and for endogenous NMDA, serotoninergic, and nicotinergic signaling in the contralateral PPTg.
机译：前防改造核（APTN）的电刺激激活两个下降疼痛抑制途径。在同侧横向植物细胞核（LPGI）中的这些途径中继之一，而对侧pedintulopontine核（PPTG）中的其他途径继电器。在啮齿动物中的各种疼痛模型中已经看到APTN刺激的抗血质效果。类似地，LPGI或PPTG刺激导致更高的疼痛阈值。已经阐明了通过电气APTN刺激激活的下降的抗血质双重途径，但尚未澄清所涉及的潜水递质机制。本研究调查了在尾部轻型试验中刺激APTN之后Ipsilidal LPGI或对侧PPTG中内源性信号传导的作用。首先，我们将大鼠提交给兴奋剂注射N-甲基-D-天冬氨酸（NMDA）进入对侧PPTG。然后，我们检查了APTN刺激诱发的镇痛（SEA）需要IPSILATELALLPGI中对NMDA（AP-7），Serotonergic（Methysergide）或阿片类药物（Naloxone）受体的阻断。同样，我们研究了NMDA，Serotonergic或Cholinergic烟碱（MeCamylamine）受体对对侧PPTG在同侧LPGI损伤大鼠的对侧PPTG上的影响。我们的结果证实，APTN刺激激活了两种疼痛抑制途径，并表明IPTN海洋中的内源性OPPGI中的内源性阿片类信号传导似乎是对侧PPTG中的内源性NMDA，血清酮和尼古丁能信号传导所必需的。

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