Ethanol inhibits voltage-gated sodium channels in cultured superior cervical ganglion neurons

Neuroreport ◽  
2008 ◽  
Vol 19 (18) ◽  
pp. 1773-1776 ◽  
Author(s):  
Zheman Xiao ◽  
Zuneng Lu ◽  
Zhongchun Liu ◽  
Wanhong Liu ◽  
Lijun Li ◽  
...  
Keyword(s):  
Sodium Channels ◽  
Superior Cervical Ganglion ◽  
Voltage Gated ◽  
Voltage Gated Sodium Channels ◽  
Cervical Ganglion ◽  
Ganglion Neurons

scholarly journals Conserved Expression of Nav1.7 and Nav1.8 Contribute to the Spontaneous and Thermally Evoked Excitability in IL-6 and NGF-Sensitized Adult Dorsal Root Ganglion Neurons In Vitro

2020 ◽  
Vol 7 (2) ◽  
pp. 44
Author(s):  
Rahul R. Atmaramani ◽  
Bryan J. Black ◽  
June Bryan de la Peña ◽  
Zachary T. Campbell ◽  
Joseph J. Pancrazio
Keyword(s):  
Sodium Channels ◽  
Sensory Neurons ◽  
Inflammatory Pain ◽  
Dorsal Root Ganglion Neurons ◽  
Electrode Arrays ◽  
Voltage Gated ◽  
Voltage Gated Sodium Channels ◽  
Ganglion Neurons

Sensory neurons respond to noxious stimuli by relaying information from the periphery to the central nervous system via action potentials driven by voltage-gated sodium channels, specifically Nav1.7 and Nav1.8. These channels play a key role in the manifestation of inflammatory pain. The ability to screen compounds that modulate voltage-gated sodium channels using cell-based assays assumes that key channels present in vivo is maintained in vitro. Prior electrophysiological work in vitro utilized acutely dissociated tissues, however, maintaining this preparation for long periods is difficult. A potential alternative involves multi-electrode arrays which permit long-term measurements of neural spike activity and are well suited for assessing persistent sensitization consistent with chronic pain. Here, we demonstrate that the addition of two inflammatory mediators associated with chronic inflammatory pain, nerve growth factor (NGF) and interleukin-6 (IL-6), to adult DRG neurons increases their firing rates on multi-electrode arrays in vitro. Nav1.7 and Nav1.8 proteins are readily detected in cultured neurons and contribute to evoked activity. The blockade of both Nav1.7 and Nav1.8, has a profound impact on thermally evoked firing after treatment with IL-6 and NGF. This work underscores the utility of multi-electrode arrays for pharmacological studies of sensory neurons and may facilitate the discovery and mechanistic analyses of anti-nociceptive compounds.

scholarly journals Modulation of Voltage-Gated Sodium Channels by Activation of Tumor Necrosis Factor Receptor-1 and Receptor-2 in Small DRG Neurons of Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
M. Leo ◽  
S. Argalski ◽  
M. Schäfers ◽  
T. Hagenacker
Keyword(s):  
Tumor Necrosis Factor ◽  
Sodium Channels ◽  
Tumor Necrosis ◽  
Dorsal Root Ganglion Neurons ◽  
Maximum Effect ◽  
Tnf Receptor ◽  
Voltage Gated ◽  
Voltage Gated Sodium Channels ◽  
Ganglion Neurons ◽  
Necrosis Factor

Tumor necrosis factor- (TNF-)αis a proinflammatory cytokine involved in the development and maintenance of inflammatory and neuropathic pain. Its effects are mediated by two receptors, TNF receptor-1 (TNFR-1) and TNF receptor-2 (TNFR-2). These receptors play a crucial role in the sensitization of voltage-gated sodium channels (VGSCs), a key mechanism in the pathogenesis of chronic pain. Using the whole-cell patch-clamp technique, we examined the influence of TNFR-1 and TNFR-2 on VGSCs and TTX-resistant NaV1.8 channels in isolated rat dorsal root ganglion neurons by using selective TNFR agonists. The TNFR-1 agonist R32W (10 pg/mL) caused an increase in the VGSC current (INa(V)) by 27.2 ± 5.1%, while the TNFR-2 agonist D145 (10 pg/mL) increased the current by 44.9 ± 2.6%. This effect was dose dependent. Treating isolated NaV1.8 with R32W (100 pg/mL) resulted in an increase inINaV(1.8)by 18.9 ± 1.6%, while treatment with D145 (100 pg/mL) increased the current by 14.5 ± 3.7%. Based on the current-voltage relationship, 10 pg of R32W or D145 led to an increase inINa(V)in a bell-shaped, voltage-dependent manner with a maximum effect at −30 mV. The effects of TNFR activation on VGSCs promote excitation in primary afferent neurons and this might explain the sensitization mechanisms associated with neuropathic and inflammatory pain.

scholarly journals Dexmedetomidine Inhibits Voltage-Gated Sodium Channels via α2-Adrenoceptors in Trigeminal Ganglion Neurons

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Sang-Taek Im ◽  
Youn Yi Jo ◽  
Gayoung Han ◽  
Hyun Jung Jo ◽  
Yong Ho Kim ◽  
...  
Keyword(s):  
G Protein ◽  
Sodium Channels ◽  
Trigeminal Ganglion ◽  
Trigeminal System ◽  
Voltage Gated ◽  
Analgesic Effects ◽  
Voltage Gated Sodium Channels ◽  
New Findings ◽  
Orofacial Region ◽  
Ganglion Neurons

Dexmedetomidine, an α2-adrenoceptor agonist, is widely used as a sedative and analgesic agent in a number of clinical applications. However, little is known about the mechanism by which it exerts its analgesic effects on the trigeminal system. Two types of voltage-gated sodium channels, Nav1.7 and Nav1.8, as well as α2-adrenoceptors are expressed in primary sensory neurons of the trigeminal ganglion (TG). Using whole-cell patch-clamp recordings, we investigated the effects of dexmedetomidine on voltage-gated sodium channel currents (INa) via α2-adrenoceptors in dissociated, small-sized TG neurons. Dexmedetomidine caused a concentration-dependent inhibition of INa in small-sized TG neurons. INa inhibition by dexmedetomidine was blocked by yohimbine, a competitive α2-adrenoceptor antagonist. Dexmedetomidine-induced inhibition of INa was mediated by G protein-coupled receptors (GPCRs) as this effect was blocked by intracellular perfusion with the G protein inhibitor GDPβ-S. Our results suggest that the INa inhibition in small-sized TG neurons, mediated by the activation of Gi/o protein-coupled α2-adrenoceptors, might contribute to the analgesic effects of dexmedetomidine in the trigeminal system. Therefore, these new findings highlight a potential novel target for analgesic drugs in the orofacial region.

Interleukin-10 down-regulates voltage gated sodium channels in rat dorsal root ganglion neurons

2013 ◽  
Vol 247 ◽  
pp. 466-475 ◽  
Author(s):  
Kai-Feng Shen ◽  
He-Quan Zhu ◽  
Xu-Hong Wei ◽  
Jun Wang ◽  
Yong-Yong Li ◽  
...  
Keyword(s):  
Dorsal Root Ganglion ◽  
Sodium Channels ◽  
Dorsal Root ◽  
Interleukin 10 ◽  
Dorsal Root Ganglion Neurons ◽  
Voltage Gated ◽  
Voltage Gated Sodium Channels ◽  
Ganglion Neurons
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