Regulation of Expression of the Sensory Neuron-Specific Sodium Channel SNS in Inflammatory and Neuropathic Pain

Increased voltage-gated sodium channel activity may contribute to the hyperexcitability of sensory neurons in inflammatory and neuropathic pain states. We examined the levels of the transcript encoding the tetrodotoxin-resistant sodium channel SNS in dorsal root ganglion neurons in a range of inflam...

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Published in:	Molecular and cellular neuroscience Vol. 10; no. 3-4; pp. 196 - 207
Main Authors:	Okuse, Kenji, Chaplan, Sandra R., McMahon, Stephen B., Luo, Z.David, Calcutt, Nigel A., Scott, Brian P., Akopian, Armen N., Wood, John N.
Format:	Journal Article
Language:	English
Published:	United States Elsevier Inc 1997
Subjects:	Animals Axotomy Cells, Cultured CHO Cells Cricetinae Diabetes Mellitus, Experimental - genetics Diabetes Mellitus, Experimental - metabolism Down-Regulation - genetics Female Freund's Adjuvant - administration & dosage Ganglia, Spinal - cytology Ganglia, Spinal - metabolism Inflammation - etiology Inflammation - genetics Inflammation - metabolism Injections, Subcutaneous Ligation Male NAV1.8 Voltage-Gated Sodium Channel Nerve Growth Factors - administration & dosage Nerve Growth Factors - pharmacology Neurons, Afferent - metabolism Pain - genetics Pain - metabolism Pain - physiopathology Rats Rats, Sprague-Dawley Rats, Wistar RNA, Messenger - analysis RNA, Messenger - drug effects RNA, Messenger - metabolism Sodium Channels - biosynthesis Sodium Channels - genetics Spinal Nerves - physiology Transcription, Genetic Up-Regulation - genetics
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Summary:	Increased voltage-gated sodium channel activity may contribute to the hyperexcitability of sensory neurons in inflammatory and neuropathic pain states. We examined the levels of the transcript encoding the tetrodotoxin-resistant sodium channel SNS in dorsal root ganglion neurons in a range of inflammatory and neuropathic pain models in the rat. Local Freund's adjuvant or systemic nerve growth factor-induced inflammation did not substantially alter the total levels of SNS mRNA. When NGF-treated adult rat DRG neuronsin vitrowere compared with NGF-depleted control neurons, SNS total mRNA levels and the levels of membrane-associated immunoreactive SNS showed a small increase (17 and 25%, respectively), while CGRP levels increased fourfold. SNS expression is thus little dependent on NGF even though SNS transcript levels dropped by more than 60% 7–14 days after axotomy. In the streptozotocin diabetic rat SNS levels fell 25%, while in several manipulations of the L5/6 tight nerve ligation rat neuropathic pain model, SNS levels fell 40–80% in rat strains that are either susceptible or relatively resistant to the development of allodynia. Increased expression of SNS mRNA is thus unlikely to underlie sensory neuron hyperexcitability associated with inflammation, while lowered SNS transcript levels are associated with peripheral nerve damage
Bibliography:	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2
ISSN:	1044-7431 1095-9327
DOI:	10.1006/mcne.1997.0657