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Antinociceptive Effects of Botulinum Toxin Type A on Trigeminal Neuropathic Pain

 K.Y. Yang  ;  M.J. Kim  ;  J.S. Ju  ;  S.K. Park  ;  C.G. Lee  ;  S.T. Kim  ;  Y.C. Bae  ;  D.K. Ahn 
 JOURNAL OF DENTAL RESEARCH, Vol.95(10) : 1183-1190, 2016 
Journal Title
Issue Date
Animals ; Botulinum Toxins, Type A/administration & dosage ; Botulinum Toxins, Type A/pharmacology* ; Disease Models, Animal ; Hyperalgesia ; Injections, Subcutaneous ; Male ; Neuralgia/drug therapy* ; Rats ; Rats, Sprague-Dawley ; Trigeminal Neuralgia/drug therapy*
allodynia ; neuropathic pain ; orofacial pain ; trigeminal nerve ; voltage dependent sodium channel
Previous studies have demonstrated that botulinum toxin type A (BoNT-A) attenuates orofacial nociception. However, there has been no evidence of the participation of the voltage-gated sodium channels (Navs) in the antinociceptive mechanisms of BoNT-A. This study investigated the cellular mechanisms underlying the antinociceptive effects of BoNT-A in a male Sprague-Dawley rat model of trigeminal neuropathic pain produced by malpositioned dental implants. The left mandibular second molar was extracted under anesthesia, followed by a miniature dental implant placement to induce injury to the inferior alveolar nerve. Mechanical allodynia was monitored after subcutaneous injection of BoNT-A at 3, 7, or 12 d after malpositioned dental implant surgery. Subcutaneous injections of 1 or 3 U/kg of BoNT-A on postoperative day 3 significantly attenuated mechanical allodynia, although 0.3 U/kg of BoNT-A did not affect the air-puff threshold. A single injection of 3 U/kg of BoNT-A produced prolonged antiallodynic effects over the entire experimental period. Treatment with BoNT-A on postoperative days 7 and 12, when pain had already been established, also produced prolonged antiallodynic effects. Double treatments with 1 U/kg of BoNT-A produced prolonged, more antiallodynic effects as compared with single treatments. Subcutaneous administration of 3 U/kg of BoNT-A significantly inhibited the upregulation of Nav isoform 1.7 (Nav1.7) expression in the trigeminal ganglion in the nerve-injured animals. These results suggest that antinociceptive effects of BoNT-A are mediated by an inhibition of upregulated Nav1.7 expression in the trigeminal ganglion. BoNT-A is therefore a potential new therapeutic agent for chronic pain control, including neuropathic pain.
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2. College of Dentistry (치과대학) > Dept. of Orofacial Pain and Oral Medicine (구강내과학교실) > 1. Journal Papers
Yonsei Authors
Kim, Seong Taek(김성택)
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