Participation of D-serine and NR2 subunits in EphA4-mediated trigeminal neuropathic pain

서지정보

ㆍ발행기관 : 대한구강생물학회 ㆍ수록지정보 : International Journal of Oral Biology / 45권 / 3호
ㆍ저자명 : Myung-Dong Kim, Min-Ji Kim, Jo-Young Son, Yu-Mi Kim, Jin-Sook Ju, Dong-Kuk Ahn

목차

Introduction
Materials and Methods
1. 실험동물
2. 악안면 신경병성통증 동물모델
3. 소뇌연수조 내 약물주입
4. 안면 이질통증의 평가
5. 면역조직화학염색
6. 통계분석
Results
Discussion
References

영어 초록

The present study investigated the participation of D-serine and NR2 in antinociception produced by blockade of central erythropoietin-producing hepatocellular carcinoma (Eph) A4 (EphA4) signaling in rats with trigeminal neuropathic pain. Trigeminal neuropathic pain was modeled in male Sprague-Dawley rats using mal-positioned dental implants. The left mandibular second molar was extracted under anesthesia, and a miniature dental implant was placed to induce injury to the inferior alveolar nerve. Our current findings showed that nerve injury induced by malpositioned dental implants significantly produced mechanical allodynia; additionally, the inferior alveolar nerve injury increased the expression of D-serine and NR2 subunits in the ipsilateral medullary dorsal horn (trigeminal subnucleus caudalis). Intracisternal administration of EphA4-Fc, an EphA4 inhibitor, inhibited nerve injury-induced mechanical allodynia and upregulated the expression of D-serine and NR2 subunits. Moreover, intracisternal administration of D-amino acids oxidase, a D-serine inhibitor, inhibited trigeminal mechanical allodynia. These results show that D-serine and NR2 subunit pathways participate in central EphA4 signaling after an inferior alveolar nerve injury. Therefore, blockade of D-serine and NR2 subunit pathways in central EphA4 signaling provides a new therapeutic target for the treatment of trigeminal neuropathic pain.

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