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J Dent Res. 2013 Dec;92(12):1113-7. doi: 10.1177/0022034513509280. Epub 2013 Oct 15.

Nitric oxide signaling contributes to ectopic orofacial neuropathic pain.

Author information

1
Department of Oral Histology, Kanagawa Dental College, 82 Inaoka-cho, Yokosuka, 238-8580, Japan.

Abstract

Inferior alveolar nerve (IAN) injury induces persistent ectopic pain which spreads to a wide area in the orofacial region. Its exact mechanism remains unclear. We investigated the involvement of nitric oxide (NO) in relation to ectopic orofacial pain caused by IAN transection (IANX). We assessed the changes in mechanical sensitivity of the whisker pad skin following IANX, neuronal nitric oxide synthase (nNOS) expression in the trigeminal ganglion (TG), and the functional significance of NO in relation to the mechanical allodynia following intra-TG administration of a chemical precursor to NO and selective nNOS inhibitors. IANX induced mechanical allodynia, which was diminished by intra-TG administration of selective nNOS inhibitors. NO metabolites and nNOS immunoreactive neurons innervating the lower lip were also increased in the TG. Intra-TG administration of nNOS substrate induced the mechanical allodynia. The present findings suggest that NO released from TG neurons regulates the excitability of TG neurons innervating the whisker pad skin, and the enhancement of TG neuronal excitability may underlie ectopic mechanical allodynia.

KEYWORDS:

7-nitroindazole; L-arginine; infraorbital nerve injury; mechanical allodynia; nitric oxide synthase; trigeminal ganglion

PMID:
24130220
DOI:
10.1177/0022034513509280
[Indexed for MEDLINE]

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