The anti-allodynic α2δ ligand pregabalin inhibits the trafficking of the calcium channel α2δ-1 subunit to presynaptic terminals in vivo

2010 ◽  
Vol 38 (2) ◽  
pp. 525-528 ◽  
Author(s):  
Claudia S. Bauer ◽  
Wahida Rahman ◽  
Alexandra Tran-Van-Minh ◽  
Rafael Lujan ◽  
Anthony H. Dickenson ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Dorsal Root ◽  
Molecular Mechanisms ◽  
Dorsal Root Ganglion Neurons ◽  
Voltage Gated ◽  
Sensory Nervous System ◽  
Pain Symptoms ◽  
Ganglion Neurons ◽  
Peripheral Sensory

Neuropathic pain is caused by lesion or dysfunction of the peripheral sensory nervous system. Up-regulation of the voltage-gated Ca2+ channel subunit α2δ-1 in DRG (dorsal root ganglion) neurons and the spinal cord correlates with the onset of neuropathic pain symptoms such as allodynia in several animal models of neuropathic pain. The clinically important anti-allodynic drugs gabapentin and pregabalin are α2δ-1 ligands, but how these drugs alleviate neuropathic pain is poorly understood. In the present paper, we review recent advances in our understanding of their molecular mechanisms.

scholarly journals Peripheral Neuropathic Pain: From Experimental Models to Potential Therapeutic Targets in Dorsal Root Ganglion Neurons

Cells ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 2725
Author(s):  
Ti-Yen Yeh ◽  
I-Wei Luo ◽  
Yu-Lin Hsieh ◽  
To-Jung Tseng ◽  
Hao Chiang ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Transcriptional Regulation ◽  
Dorsal Root ◽  
Molecular Mechanisms ◽  
Dorsal Root Ganglion Neurons ◽  
Peripheral Sensitization ◽  
Post Translational Modification ◽  
Peripheral Neuropathic Pain ◽  
Pain Models ◽  
Ganglion Neurons

Neuropathic pain exerts a global burden caused by the lesions in the somatosensory nerve system, including the central and peripheral nervous systems. The mechanisms of nerve injury-induced neuropathic pain involve multiple mechanisms, various signaling pathways, and molecules. Currently, poor efficacy is the major limitation of medications for treating neuropathic pain. Thus, understanding the detailed molecular mechanisms should shed light on the development of new therapeutic strategies for neuropathic pain. Several well-established in vivo pain models were used to investigate the detail mechanisms of peripheral neuropathic pain. Molecular mediators of pain are regulated differentially in various forms of neuropathic pain models; these regulators include purinergic receptors, transient receptor potential receptor channels, and voltage-gated sodium and calcium channels. Meanwhile, post-translational modification and transcriptional regulation are also altered in these pain models and have been reported to mediate several pain related molecules. In this review, we focus on molecular mechanisms and mediators of neuropathic pain with their corresponding transcriptional regulation and post-translational modification underlying peripheral sensitization in the dorsal root ganglia. Taken together, these molecular mediators and their modification and regulations provide excellent targets for neuropathic pain treatment.

scholarly journals 902. Modulation of Voltage-Gated Potassium Channels in Dorsal Root Ganglion Neurons by an Inducible Adenoviral Vector In Vivo

2006 ◽  
Vol 13 ◽  
pp. S347-S348 ◽  
Author(s):  
Chao Ma ◽  
Robert H. LaMotte ◽  
Jason M. Rosenzweig ◽  
Peter L. Gehlbach ◽  
David C. Johns
Keyword(s):  
Dorsal Root Ganglion ◽  
Potassium Channels ◽  
Dorsal Root ◽  
Adenoviral Vector ◽  
Dorsal Root Ganglion Neurons ◽  
Voltage Gated ◽  
Ganglion Neurons

scholarly journals Temporal mechanically-induced signaling events in bone and dorsal root ganglion neurons after in vivo bone loading

PLoS ONE ◽  
2018 ◽  
Vol 13 (2) ◽  
pp. e0192760
Author(s):  
Jason A. Bleedorn ◽  
Troy A. Hornberger ◽  
Craig A. Goodman ◽  
Zhengling Hao ◽  
Susannah J. Sample ◽  
...  
Keyword(s):  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
Signaling Events ◽  
Bone Loading ◽  
Ganglion Neurons
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