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.

이상의 실험결과들을 요약하면, CFA를 안면영역 피하로 주입하여 발생한 염증성 통증 행위반응은 P2X 수용체의 억제제의 투여로 감소할 수 있었다. 특히 P2X7 수용체 억제제를 투여하면 진통작용 뿐 아니라 활성화된 신경아교세포 발현을 억제하였다. 이러한 실험 결과는 P2X7 수용체가 신경아교세포에 영향을 미쳐 안면에서 발생하는 만성 염증성 통증의 발생과 유지에 관여하고 있다는 것을 보여준다. 따라서 중추신경계의 신경아교세포를 조절할 수 있는 중추성 P2X7 수용체 작용기전은 임상에서 만성 염증성 통증을 보다 효과적으로 치료할 수 있는 새로운 방법을 제시해 줄 수 있다고 생각된다.

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