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内侧隔区谷氨酸能神经元通过投射至下丘脑外侧来调节慢性神经性疼痛中的伤害感受。

Medial septum glutamatergic neurons modulate nociception in chronic neuropathic pain via projections to lateral hypothalamus.

作者信息

Fan Bing-Qian, Xia Jun-Ming, Chen Dan-Dan, Feng Li-Li, Ding Jia-Hui, Li Shuang-Shuang, Li Wen-Xian, Han Yuan

机构信息

Department of Anesthesiology, The Eye and ENT Hospital of Fudan University, Shanghai, China.

出版信息

Front Pharmacol. 2023 May 17;14:1171665. doi: 10.3389/fphar.2023.1171665. eCollection 2023.

DOI:10.3389/fphar.2023.1171665
PMID:37266154
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10229799/
Abstract

The medial septum (MS) contributes in pain processing and regulation, especially concerning persistent nociception. However, the role of MS glutamatergic neurons in pain and the underlying neural circuit mechanisms in pain remain poorly understood. In this study, chronic constrictive injury of the sciatic nerve (CCI) surgery was performed to induce thermal and mechanical hyperalgesia in mice. The chemogenetic activation of MS glutamatergic neurons decreased pain thresholds in naïve mice. In contrast, inhibition or ablation of these neurons has improved nociception thresholds in naïve mice and relieved thermal and mechanical hyperalgesia in CCI mice. Anterograde viral tracing revealed that MS glutamatergic neurons had projections to the lateral hypothalamus (LH) and supramammillary nucleus (SuM). We further demonstrated that MS glutamatergic neurons regulate pain thresholds by projecting to LH but not SuM, because the inhibition of MS-LH glutamatergic projections suppressed pain thresholds in CCI and naïve mice, yet, optogenetic activation or inhibition of MS-SuM glutamatergic projections had no effect on pain thresholds in naïve mice. In conclusion, our results reveal that MS glutamatergic neurons play a significant role in regulating pain perception and decipher that MS glutamatergic neurons modulate nociception via projections to LH.

摘要

内侧隔区（MS）参与疼痛的处理和调节，尤其是在持续性伤害感受方面。然而，MS谷氨酸能神经元在疼痛中的作用以及疼痛潜在的神经回路机制仍知之甚少。在本研究中，进行坐骨神经慢性缩窄损伤（CCI）手术以诱导小鼠出现热痛觉过敏和机械性痛觉过敏。对MS谷氨酸能神经元进行化学遗传激活会降低未处理小鼠的疼痛阈值。相反，抑制或消除这些神经元可提高未处理小鼠的伤害感受阈值，并减轻CCI小鼠的热痛觉过敏和机械性痛觉过敏。顺行病毒示踪显示，MS谷氨酸能神经元投射至外侧下丘脑（LH）和乳头体上核（SuM）。我们进一步证明，MS谷氨酸能神经元通过投射至LH而非SuM来调节疼痛阈值，因为抑制MS-LH谷氨酸能投射会降低CCI小鼠和未处理小鼠的疼痛阈值，然而，对MS-SuM谷氨酸能投射进行光遗传学激活或抑制对未处理小鼠的疼痛阈值没有影响。总之，我们的结果表明，MS谷氨酸能神经元在调节疼痛感知中起重要作用，并阐明MS谷氨酸能神经元通过投射至LH来调节伤害感受。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4280/10229799/66bbb9bf785f/fphar-14-1171665-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4280/10229799/66bbb9bf785f/fphar-14-1171665-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4280/10229799/065026eaaa0a/fphar-14-1171665-g001.jpg
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