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Nav1.3在神经病理性疼痛中的作用机制 被引量:1
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作者 杨彬彬 王冬梅 《中国疼痛医学杂志》 CAS CSCD 北大核心 2023年第2期120-126,共7页
Nav1.3是电压门控钠离子通道亚型之一,由SCN3A基因编码,对河豚毒素(tetrodotoxin,TTX)敏感。Nav1.3通道电流具有快速激活、快速失活和快速由失活状态恢复维持高频放电的特征,可在慢斜坡去极化期间被激活并产生持续钠电流,放大神经元兴奋... Nav1.3是电压门控钠离子通道亚型之一,由SCN3A基因编码,对河豚毒素(tetrodotoxin,TTX)敏感。Nav1.3通道电流具有快速激活、快速失活和快速由失活状态恢复维持高频放电的特征,可在慢斜坡去极化期间被激活并产生持续钠电流,放大神经元兴奋性,在神经电信号的产生及传导过程中起着重要作用。研究发现Nav1.3的错义突变与部分神经损伤引起的电流变化具有共性,通过多种方式导致神经元异常放电,参与并调控痛觉过敏的发生。本文对Nav1.3参与神经病理性疼痛有关机制进行综述,探讨神经部位Nav1.3的表达变化与痛敏表型之间的关系、各种细胞因子及其受体调控Nav1.3的上下游信号及不同病理性疼痛变化差异的比较等,分析Nav1.3在神经病理性疼痛中的作用及其机制,探讨Nav1.3成为镇痛靶点的可能性。 展开更多
关键词 电压门控钠通道亚型 nav1.3 神经病理性疼痛 镇痛
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Nav1.3对RIN-14B细胞兴奋性的调控作用
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作者 韩林慧 龚华珊 +2 位作者 朱翠红 张国花 戎伟芳 《上海交通大学学报(医学版)》 CAS CSCD 北大核心 2019年第2期142-146,共5页
目的·用电生理学方法证明RIN-14B细胞是一种可用的肠嗜铬细胞(enterochromaffin cells, EC)模型;明确Nav1.3通道在其兴奋性调控中的作用。方法·在传代培养的RIN-14B细胞中,用电流钳记录静息电位,观察给予河豚毒素(tetrodotoxi... 目的·用电生理学方法证明RIN-14B细胞是一种可用的肠嗜铬细胞(enterochromaffin cells, EC)模型;明确Nav1.3通道在其兴奋性调控中的作用。方法·在传代培养的RIN-14B细胞中,用电流钳记录静息电位,观察给予河豚毒素(tetrodotoxin,TTX)和Nav1.3阻断剂ICA-121431后电位变化;用电压钳记录Na^+电流,观察给予TTX和ICA-121431后电流变化。结果·RIN-14B细胞静息膜电位约为-60 mV,在去极化刺激下发放动作电位。TTX可以完全阻断动作电位,而ICA-121431可以浓度依赖性地抑制动作电位。钠通道的激活电流和失活电流被TTX完全阻断,激活电流被ICA-121431浓度依赖性抑制。结论·RIN-14B细胞是一种可兴奋细胞,TTX敏感型的钠通道介导其动作电位的发放,Nav1.3参与调控其兴奋性,与EC特征相似;说明RIN-14B细胞是一种良好的EC模型。 展开更多
关键词 RIN-14B细胞 钠通道亚型nav1.3 肠嗜铬细胞 河豚毒素 ICA-121431
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Transforming growth factor-beta 1 enhances discharge activity of cortical neurons
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作者 Zhihui Ren Tian Li +5 位作者 Xueer Liu Zelin Zhang Xiaoxuan Chen Weiqiang Chen Kangsheng Li Jiangtao Sheng 《Neural Regeneration Research》 SCIE CAS 2025年第2期548-556,共9页
Transforming growth factor-beta 1(TGF-β1)has been extensively studied for its pleiotropic effects on central nervous system diseases.The neuroprotective or neurotoxic effects of TGF-β1 in specific brain areas may de... Transforming growth factor-beta 1(TGF-β1)has been extensively studied for its pleiotropic effects on central nervous system diseases.The neuroprotective or neurotoxic effects of TGF-β1 in specific brain areas may depend on the pathological process and cell types involved.Voltage-gated sodium channels(VGSCs)are essential ion channels for the generation of action potentials in neurons,and are involved in various neuroexcitation-related diseases.However,the effects of TGF-β1 on the functional properties of VGSCs and firing properties in cortical neurons remain unclear.In this study,we investigated the effects of TGF-β1 on VGSC function and firing properties in primary cortical neurons from mice.We found that TGF-β1 increased VGSC current density in a dose-and time-dependent manner,which was attributable to the upregulation of Nav1.3 expression.Increased VGSC current density and Nav1.3 expression were significantly abolished by preincubation with inhibitors of mitogen-activated protein kinase kinase(PD98059),p38 mitogen-activated protein kinase(SB203580),and Jun NH2-terminal kinase 1/2 inhibitor(SP600125).Interestingly,TGF-β1 significantly increased the firing threshold of action potentials but did not change their firing rate in cortical neurons.These findings suggest that TGF-β1 can increase Nav1.3 expression through activation of the ERK1/2-JNK-MAPK pathway,which leads to a decrease in the firing threshold of action potentials in cortical neurons under pathological conditions.Thus,this contributes to the occurrence and progression of neuroexcitatory-related diseases of the central nervous system. 展开更多
关键词 central nervous system cortical neurons ERK firing properties JNK nav1.3 p38 transforming growth factor-beta 1 traumatic brain injury voltage-gated sodium currents
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Modulatory effect of auxiliary β_1 subunit on Nav1.3 voltage-gated sodium channel expressed in Xenopus oocyte
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作者 WANG Ying-wei CHENG Zhi-jun +3 位作者 TAN Hong XIA Yi-meng REN Rong-rong DING Yu-qiang 《Chinese Medical Journal》 SCIE CAS CSCD 2007年第8期721-723,共3页
Voltage-gated sodium channels play an important role in the generation and propagation of action potentials in excitable cells. They are composed of a pore-forming α subunit and auxiliary β subunits. To date, nine s... Voltage-gated sodium channels play an important role in the generation and propagation of action potentials in excitable cells. They are composed of a pore-forming α subunit and auxiliary β subunits. To date, nine subtypes of the α subunit, designated Nav1.1 to Nav1.9, have been shown to form functional sodium channels. In addition, four different mammalian subunits (β1-β4) isoforms have been cloned from the nervous system. The β subunits are structurally homologous and form single transmembrane glycoproteins with short intracellular loops and immunoglobulin-like extracellular segments. The association of the various α subtypes with different combinations of auxiliary β subunits creates the possibility of additional molecular and functional complexity for neuronal sodium channels. 展开更多
关键词 nav1.3 sodium channel β subunit OOCYTE neuropathic pain
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电压门控钠通道在慢性疼痛药物发现中的研究进展 被引量:1
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作者 羊健 杨清云 +2 位作者 孙水根 冯怡 张继全 《安徽医药》 CAS 2023年第1期5-9,共5页
由于发病率高、药物效果有限或治疗药物受限等原因,慢性疼痛的治疗一直是世界范围内研究人员关注的难题。电压门控钠通道(VGSCs)阻滞剂有较为显著的镇痛作用,目前已知与慢性疼痛相关的钠通道亚型主要有Nav1.3、Nav1.7、Nav1.8、Nav1.9。... 由于发病率高、药物效果有限或治疗药物受限等原因,慢性疼痛的治疗一直是世界范围内研究人员关注的难题。电压门控钠通道(VGSCs)阻滞剂有较为显著的镇痛作用,目前已知与慢性疼痛相关的钠通道亚型主要有Nav1.3、Nav1.7、Nav1.8、Nav1.9。2021年8—9月进行了该研究,全面概括了上述钠通道亚型与慢性疼痛的关系,归纳出潜在候选药物临床前研究方法,以及已被证实安全有效的选择性钠通道阻滞剂品种,为选择性钠通道阻滞剂的开发提供参考。 展开更多
关键词 慢性疼痛 镇痛药 电压门控钠通道阻滞剂 NAV1.1电压门控钠通道 nav1.3电压门控钠通道 NAV1.7电压门控钠通道 NAV1.8电压门控钠通道 NAV1.9电压门控钠通道 综述
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外周神经损伤引起病理性疼痛的机制 被引量:29
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作者 刘先国 《中山大学学报(医学科学版)》 CAS CSCD 北大核心 2009年第6期641-644,651,共5页
外周神经损伤往往导致慢性疼痛,即神经病理性疼痛。大量的研究表明,神经损伤主要通过使初级感觉神经元产生自发放电(即异位冲动)和脊髓背角突触传递效率的持续性增强(即LTP)导致病理性疼痛。近年来的研究表明,致炎细胞因子TNF-α在神经... 外周神经损伤往往导致慢性疼痛,即神经病理性疼痛。大量的研究表明,神经损伤主要通过使初级感觉神经元产生自发放电(即异位冲动)和脊髓背角突触传递效率的持续性增强(即LTP)导致病理性疼痛。近年来的研究表明,致炎细胞因子TNF-α在神经病理性疼痛中起重要作用。神经损伤可通过上调TNF-α,导致初级感觉神经元上Nav1.3和Nav1.8过表达,引起异位冲动。TNF-α的上调还可显著易化脊髓背角C纤维诱发电位的LTP。由于TNF-α的上调,Nav1.3和Nav1.8过表达和脊髓背角LTP的形成主要与运动神经损伤相关,因此运动神经损伤可能是引起病理性疼痛的主要原因。 展开更多
关键词 神经病理性疼痛 异位冲动 背根神经节 长时程增强 脊髓背角 TNF—α nav1.3 NAV1.8 运动神经损伤
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Pharmacological kinetics of BmK AS, a sodium channel site 4-specific modulator on Na_v1.3 被引量:5
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作者 Zhi-Rui Liu Jie Tao +4 位作者 Bang-Qian Dong Gang Ding Zhi-Jun Cheng Hui-Qiong He Yong-Hua Ji 《Neuroscience Bulletin》 SCIE CAS CSCD 2012年第3期209-221,共13页
Objective In this study, the pharmacological kinetics of Buthus martensi Karsch (BmK) AS, a specific modulator of voltage-gated sodium channel site 4, was investigated on Nav1.3 expressed in Xenopus oocytes. Methods... Objective In this study, the pharmacological kinetics of Buthus martensi Karsch (BmK) AS, a specific modulator of voltage-gated sodium channel site 4, was investigated on Nav1.3 expressed in Xenopus oocytes. Methods Two-electrode voltage clamp was used to record the whole-cell sodium current. Results The peak currents of Nav1.3 were depressed by BmK AS over a wide range of concentrations (10, 100, and 500 nmol/L). Most remarkably, BmK AS at 100 nmol/L hyperpolarized the voltage-dependence and increased the voltage-sensitivity of steady-state activation/inactivation. In addition, BmK AS was capable of hyperpolarizing not only the fast inactivation but also the slow inactivation, with a greater preference for the latter. Moreover, BmK AS accelerated the time constant and increased the ratio of recovery in Nav1.3 at all concentrations. Conclusion This study provides direct evidence that BmK AS facilitates steady-state activation and inhibits slow inactivation by stabilizing both the closed and open states of the Nav1.3 channel, which might result from an integrative binding to two receptor sites on the voltage-gated sodium channels. These results may shed light on therapeutics against Nav1.3-targeted pathology. 展开更多
关键词 VGSC subtype nav1.3 VGSC site 4-specific modulator BmKAS
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