• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

Nav1.9 通道对肠道高反应性和运动障碍的影响。

The influence of Nav1.9 channels on intestinal hyperpathia and dysmotility.

机构信息

Department of Gastroenterology, Henan Provincial People's Hospital, Zhengzhou University People's Hospital, Zhengzhou, China.

Department of Gastroenterology, The Second Xiangya Hospital, Central South University, Changsha, China.

出版信息

Channels (Austin). 2023 Dec;17(1):2212350. doi: 10.1080/19336950.2023.2212350.

DOI:10.1080/19336950.2023.2212350
PMID:37186898
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10187076/
Abstract

The Nav1.9 channel is a voltage-gated sodium channel. It plays a vital role in the generation of pain and the formation of neuronal hyperexcitability after inflammation. It is highly expressed in small diameter neurons of dorsal root ganglions and Dogiel II neurons in enteric nervous system. The small diameter neurons in dorsal root ganglions are the primary sensory neurons of pain conduction. Nav1.9 channels also participate in regulating intestinal motility. Functional enhancements of Nav1.9 channels to a certain extent lead to hyperexcitability of small diameter dorsal root ganglion neurons. The hyperexcitability of the neurons can cause visceral hyperalgesia. Intestinofugal afferent neurons and intrinsic primary afferent neurons in enteric nervous system belong to Dogiel type II neurons. Their excitability can also be regulated by Nav1.9 channels. The hyperexcitability of intestinofugal afferent neurons abnormally activate entero-enteric inhibitory reflexes. The hyperexcitability of intrinsic primary afferent neurons disturb peristaltic waves by abnormally activating peristaltic reflexes. This review discusses the role of Nav1.9 channels in intestinal hyperpathia and dysmotility.

摘要

Nav1.9 通道是一种电压门控钠离子通道。它在炎症后疼痛的产生和神经元兴奋性增高的形成中起着至关重要的作用。它在背根神经节的小直径神经元和肠神经系统中的 Dogiel II 神经元中高度表达。背根神经节的小直径神经元是疼痛传导的主要感觉神经元。Nav1.9 通道也参与调节肠道运动。Nav1.9 通道的功能增强在一定程度上导致小直径背根神经节神经元的兴奋性增高。神经元的兴奋性增高可导致内脏痛觉过敏。肠传出神经元和肠神经系统中的内在初级传入神经元属于 Dogiel Ⅱ型神经元。它们的兴奋性也可以被 Nav1.9 通道调节。肠传出神经元的兴奋性增高异常激活肠-肠抑制反射。内在初级传入神经元的兴奋性增高通过异常激活蠕动反射扰乱蠕动波。本文综述了 Nav1.9 通道在肠道高敏性和运动障碍中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1c/10187076/b92431e94903/KCHL_A_2212350_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1c/10187076/d67fdd34a34b/KCHL_A_2212350_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1c/10187076/bb773cf6b7ca/KCHL_A_2212350_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1c/10187076/18a869c8890b/KCHL_A_2212350_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1c/10187076/b92431e94903/KCHL_A_2212350_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1c/10187076/d67fdd34a34b/KCHL_A_2212350_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1c/10187076/bb773cf6b7ca/KCHL_A_2212350_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1c/10187076/18a869c8890b/KCHL_A_2212350_F0003_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1b1c/10187076/b92431e94903/KCHL_A_2212350_F0004_OC.jpg

相似文献

1
The influence of Nav1.9 channels on intestinal hyperpathia and dysmotility.Nav1.9 通道对肠道高反应性和运动障碍的影响。
Channels (Austin). 2023 Dec;17(1):2212350. doi: 10.1080/19336950.2023.2212350.
2
The Gain-of-Function R222S Variant in Contributes to Visceral Hyperalgesia and Intestinal Dysmotility in 11 Mice.功能获得性R222S变体导致11只小鼠出现内脏痛觉过敏和肠道运动障碍。
Front Neurol. 2022 May 27;13:856459. doi: 10.3389/fneur.2022.856459. eCollection 2022.
3
Contribution of the tetrodotoxin-resistant voltage-gated sodium channel NaV1.9 to sensory transmission and nociceptive behavior.河豚毒素抗性电压门控钠通道NaV1.9对感觉传递和伤害性感受行为的作用。
Proc Natl Acad Sci U S A. 2005 Jun 28;102(26):9382-7. doi: 10.1073/pnas.0501549102. Epub 2005 Jun 17.
4
Chronic exposure to tumor necrosis factor in vivo induces hyperalgesia, upregulates sodium channel gene expression and alters the cellular electrophysiology of dorsal root ganglion neurons.体内长期暴露于肿瘤坏死因子会诱发痛觉过敏,上调钠通道基因表达,并改变背根神经节神经元的细胞电生理学特性。
Neurosci Lett. 2017 Jul 13;653:195-201. doi: 10.1016/j.neulet.2017.05.004. Epub 2017 May 27.
5
Painful and painless mutations of SCN9A and SCN11A voltage-gated sodium channels.电压门控钠离子通道 SCN9A 和 SCN11A 的疼痛和无痛突变。
Pflugers Arch. 2020 Jul;472(7):865-880. doi: 10.1007/s00424-020-02419-9. Epub 2020 Jun 29.
6
Bulleyaconitine A attenuates hyperexcitability of dorsal root ganglion neurons induced by spared nerve injury: The role of preferably blocking Nav1.7 and Nav1.3 channels.草乌甲素 A 减轻 spared nerve injury 诱导的背根神经节神经元过度兴奋:优选阻断 Nav1.7 和 Nav1.3 通道的作用。
Mol Pain. 2018 Jan-Dec;14:1744806918778491. doi: 10.1177/1744806918778491.
7
Specialized functions of Nav1.5 and Nav1.9 channels in electrogenesis of myenteric neurons in intact mouse ganglia.Nav1.5 和 Nav1.9 通道在完整小鼠神经节中肠神经元发电中的专门功能。
J Neurosci. 2014 Apr 9;34(15):5233-44. doi: 10.1523/JNEUROSCI.0057-14.2014.
8
Upregulation of sodium channel Nav1.3 and functional involvement in neuronal hyperexcitability associated with central neuropathic pain after spinal cord injury.脊髓损伤后中枢神经性疼痛相关的钠通道Nav1.3上调及其在神经元过度兴奋中的功能作用。
J Neurosci. 2003 Oct 1;23(26):8881-92. doi: 10.1523/JNEUROSCI.23-26-08881.2003.
9
Dissecting the role of sodium currents in visceral sensory neurons in a model of chronic hyperexcitability using Nav1.8 and Nav1.9 null mice.利用Nav1.8和Nav1.9基因敲除小鼠,剖析慢性兴奋性过高模型中内脏感觉神经元钠电流的作用。
J Physiol. 2006 Oct 1;576(Pt 1):257-67. doi: 10.1113/jphysiol.2006.113597. Epub 2006 Jul 20.
10
Spider venom-derived peptide induces hyperalgesia in Na1.7 knockout mice by activating Na1.9 channels.蜘蛛毒液衍生肽通过激活 Na1.9 通道在 Na1.7 敲除小鼠中引起痛觉过敏。
Nat Commun. 2020 May 8;11(1):2293. doi: 10.1038/s41467-020-16210-y.

引用本文的文献

1
Clinical efficacy and regulatory mechanisms of Shi Pi Zeng Ye formula in treating functional constipation comorbid with depression: integrating clinical observation, mass spectrometry, bioinformatics, and molecular docking.实脾增液方治疗功能性便秘合并抑郁的临床疗效及调控机制:整合临床观察、质谱分析、生物信息学和分子对接
Front Pharmacol. 2025 Aug 20;16:1645277. doi: 10.3389/fphar.2025.1645277. eCollection 2025.
2
Gut sensory neurons as regulators of neuro-immune-microbial interactions: from molecular mechanisms to precision therapy for IBD/IBS.肠道感觉神经元作为神经-免疫-微生物相互作用的调节因子:从分子机制到炎症性肠病/肠易激综合征的精准治疗
J Neuroinflammation. 2025 Jul 2;22(1):172. doi: 10.1186/s12974-025-03500-9.
3

本文引用的文献

1
The Gain-of-Function R222S Variant in Contributes to Visceral Hyperalgesia and Intestinal Dysmotility in 11 Mice.功能获得性R222S变体导致11只小鼠出现内脏痛觉过敏和肠道运动障碍。
Front Neurol. 2022 May 27;13:856459. doi: 10.3389/fneur.2022.856459. eCollection 2022.
2
A Novel Spider Toxin Inhibits Fast Inactivation of the Na1.9 Channel by Binding to Domain III and Domain IV Voltage Sensors.一种新型蜘蛛毒素通过结合结构域III和结构域IV电压传感器来抑制Na1.9通道的快速失活。
Front Pharmacol. 2021 Dec 6;12:778534. doi: 10.3389/fphar.2021.778534. eCollection 2021.
3
Tetrodotoxin, a Potential Drug for Neuropathic and Cancer Pain Relief?
Sensory neuron sodium channels as pain targets; from cocaine to Journavx (VX-548, suzetrigine).
作为疼痛靶点的感觉神经元钠通道;从可卡因到Journavx(VX-548,舒泽曲明)。
J Gen Physiol. 2025 Jul 7;157(4). doi: 10.1085/jgp.202513778. Epub 2025 Apr 28.
4
exploration of bioactive secondary metabolites with anesthetic effects on sodium channels Nav 1.7, 1.8, and 1.9 in painful human dental pulp.对人疼痛牙髓中对钠通道Nav 1.7、1.8和1.9有麻醉作用的生物活性次生代谢产物的探索。
Mol Pain. 2025 Jan-Dec;21:17448069251327824. doi: 10.1177/17448069251327824. Epub 2025 Mar 11.
5
Exploring novel non-opioid pathways and therapeutics for pain modulation.探索用于疼痛调节的新型非阿片类途径和疗法。
Mol Pain. 2025 Jan-Dec;21:17448069251327840. doi: 10.1177/17448069251327840. Epub 2025 Mar 11.
6
Genetic Analysis of , , and in Familial Episodic Pain Syndrome (FEPS) in Japan and Proposal of Clinical Diagnostic Criteria.遗传性家族性发作性疼痛综合征(FEPS)中 、 、 的基因分析及临床诊断标准的建立。
Int J Mol Sci. 2024 Jun 21;25(13):6832. doi: 10.3390/ijms25136832.
河豚毒素,一种用于缓解神经性和癌性疼痛的潜在药物?
Toxins (Basel). 2021 Jul 12;13(7):483. doi: 10.3390/toxins13070483.
4
The role of enteric inhibitory neurons in intestinal motility.肠抑制神经元在肠道运动中的作用。
Auton Neurosci. 2021 Nov;235:102854. doi: 10.1016/j.autneu.2021.102854. Epub 2021 Jul 17.
5
Post-infection Irritable Bowel Syndrome.感染后肠易激综合征。
Gastroenterol Clin North Am. 2021 Jun;50(2):445-461. doi: 10.1016/j.gtc.2021.02.007. Epub 2021 Apr 23.
6
Sisters with No Pain, No Tears: A Report of a New Variant of Hereditary Sensory and Autonomic Neuropathy (Type IX) Caused by a Novel SCN11A Mutation.无痛无泪的姐妹:一例由新型SCN11A突变引起的遗传性感觉和自主神经病变(IX型)新变体报告
Indian J Dermatol. 2020 Jul-Aug;65(4):299-303. doi: 10.4103/ijd.IJD_416_18.
7
Gain-of-function mutation in SCN11A causes itch and affects neurogenic inflammation and muscle function in Scn11a+/L799P mice.SCN11A 获得性功能突变引起瘙痒,并影响 Scn11a+/L799P 小鼠的神经源性炎症和肌肉功能。
PLoS One. 2020 Aug 20;15(8):e0237101. doi: 10.1371/journal.pone.0237101. eCollection 2020.
8
[Unique characteristics of "the second brain" - The enteric nervous system].["“第二大脑”的独特特征——肠神经系统"]
Sheng Li Xue Bao. 2020 Jun 25;72(3):382-390.
9
Pharmacological activity and NMR solution structure of the leech peptide HSTX-I.水蛭肽 HSTX-I 的药理学活性和 NMR 溶液结构。
Biochem Pharmacol. 2020 Nov;181:114082. doi: 10.1016/j.bcp.2020.114082. Epub 2020 Jun 7.
10
Functional circuits and signal processing in the enteric nervous system.肠神经系统中的功能回路和信号处理。
Cell Mol Life Sci. 2020 Nov;77(22):4505-4522. doi: 10.1007/s00018-020-03543-6. Epub 2020 May 18.