Journal
NEUROSCIENCE BULLETIN
Volume 34, Issue 1, Pages 4-12Publisher
SPRINGER
DOI: 10.1007/s12264-017-0132-3
Keywords
Dorsal root ganglion; Neuropathic pain; Paclitaxel; Voltage-gated sodium channels
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Funding
- NIH [NS87988, DE17794, DE22743, NS89479]
- NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH [R01DE017794, R01DE022743] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS089479, R01NS087988] Funding Source: NIH RePORTER
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Voltage-gated sodium channels (Navs) play an important role in human pain sensation. However, the expression and role of Nav subtypes in native human sensory neurons are unclear. To address this issue, we obtained human dorsal root ganglion (hDRG) tissues from healthy donors. PCR analysis of seven DRG-expressed Nav subtypes revealed that the hDRG has higher expression of Nav1.7 (50% of total Nav expression) and lower expression of Nav1.8 (12%), whereas the mouse DRG has higher expression of Nav1.8 (45%) and lower expression of Nav1.7 (18%). To mimic Nav regulation in chronic pain, we treated hDRG neurons in primary cultures with paclitaxel (0.1-1 mu mol/L) for 24 h. Paclitaxel increased the Nav1.7 but not Nav1.8 expression and also increased the transient Na+ currents and action potential firing frequency in small-diameter (< 50 mu m) hDRG neurons. Thus, the hDRG provides a translational model in which to study human pain in a dish and test new pain therapeutics.
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