Preemptive application of QX-314 attenuates trigeminal neuropathic mechanical allodynia in rats.
10.4196/kjpp.2018.22.3.331
- Author:
Jeong Ho YOON
1
;
Jo Young SON
;
Min Ji KIM
;
Song Hee KANG
;
Jin Sook JU
;
Yong Chul BAE
;
Dong Kuk AHN
Author Information
1. Department of Oral Physiology School of Dentistry, Kyungpook National University, Daegu 41940, Korea. dkahn@knu.ac.kr
- Publication Type:Original Article
- Keywords:
Mechanical allodynia;
Preemptive analgesia;
QX-314;
Sodium channel;
Trigeminal neuropathic pain
- MeSH:
Analgesia;
Animals;
Constriction;
Humans;
Hyperalgesia*;
Male;
Neuralgia;
Neurons;
Rats*;
Rats, Sprague-Dawley;
Sodium Channels;
Trigeminal Ganglion;
Up-Regulation;
Voltage-Gated Sodium Channels
- From:The Korean Journal of Physiology and Pharmacology
2018;22(3):331-341
- CountryRepublic of Korea
- Language:English
-
Abstract:
The aim of the present study was to examine the effects of preemptive analgesia on the development of trigeminal neuropathic pain. For this purpose, mechanical allodynia was evaluated in male Sprague-Dawley rats using chronic constriction injury of the infraorbital nerve (CCI-ION) and perineural application of 2% QX-314 to the infraorbital nerve. CCI-ION produced severe mechanical allodynia, which was maintained until postoperative day (POD) 30. An immediate single application of 2% QX-314 to the infraorbital nerve following CCI-ION significantly reduced neuropathic mechanical allodynia. Immediate double application of QX-314 produced a greater attenuation of mechanical allodynia than a single application of QX-314. Immediate double application of 2% QX-314 reduced the CCI-ION-induced upregulation of GFAP and p-p38 expression in the trigeminal ganglion. The upregulated p-p38 expression was co-localized with NeuN, a neuronal cell marker. We also investigated the role of voltage-gated sodium channels (Navs) in the antinociception produced by preemptive application of QX-314 through analysis of the changes in Nav expression in the trigeminal ganglion following CCI-ION. Preemptive application of QX-314 significantly reduced the upregulation of Nav1.3, 1.7, and 1.9 produced by CCI-ION. These results suggest that long-lasting blockade of the transmission of pain signaling inhibits the development of neuropathic pain through the regulation of Nav isoform expression in the trigeminal ganglion. Importantly, these results provide a potential preemptive therapeutic strategy for the treatment of neuropathic pain after nerve injury.
