Sarıtaş Zülfükar Kadir, Börü Ülkü Türk, Erdoğan Metin, Bölük Cem, Özbek Fatma Görücü, Acar Hakan, Koç Yusuf, İncebacak Furkan
Department of Surgery, Faculty of Veterinary Medicine, University of Afyon Kocatepe, Afyonkarahisar, Türkiye.
Department of Neurology, University of Afyonkarahisar Health Sciences, Afyonkarahisar, Türkiye.
Sci Prog. 2025 Jul-Sep;108(3):368504251376909. doi: 10.1177/00368504251376909. Epub 2025 Sep 9.
A considerable number of individuals are diagnosed with idiopathic trigeminal neuralgia. In order to achieve a more complete understanding of the pathophysiology, it is essential to adopt a range of novel approaches and utilize new animal models. This study investigated changes in the messenger RNA (mRNA) expression of ion-channels in a newly developed animal model of trigeminal neuropathic pain induced by cervical spinal dorsal horn compression. Eighteen rabbits were randomly assigned into three groups (spinal cord compression, sham, and control groups), and a previously developed animal model was applied. Quantitative polymerase chain reaction was applied to examine the genetic expression of Na, K, and Ca channels in the cervical dorsal horn, trigeminal ganglion, and infraorbital nerve. The mRNA expression levels of SCN8A and SCN9A exhibited a marked increase in the infraorbital nerve of the spinal cord compression group when compared to the sham group. Furthermore, the mRNA expression levels of CACNA1C, KCNK1, and SCN9A demonstrated a significant increase in all investigated regions when compared to the control group. The present findings indicate the potential critical involvement of Nav1.6 and Nav1.7 in the pathogenesis of trigeminal neuropathic pain. However, the potential involvement of the CaV2.1, CaV1.2, and K2P1.1 channels cannot be ruled out at this juncture.
相当多的个体被诊断为特发性三叉神经痛。为了更全面地了解其病理生理学，采用一系列新方法并利用新的动物模型至关重要。本研究调查了在一种新开发的由颈脊髓背角压迫诱导的三叉神经病理性疼痛动物模型中离子通道信使核糖核酸（mRNA）表达的变化。18只兔子被随机分为三组（脊髓压迫组、假手术组和对照组），并应用了先前开发的动物模型。采用定量聚合酶链反应检测颈背角、三叉神经节和眶下神经中钠、钾和钙通道的基因表达。与假手术组相比，脊髓压迫组眶下神经中SCN8A和SCN9A的mRNA表达水平显著升高。此外，与对照组相比，所有研究区域中CACNA1C、KCNK1和SCN9A的mRNA表达水平均显著升高。本研究结果表明Nav1.6和Nav1.7在三叉神经病理性疼痛的发病机制中可能起关键作用。然而，目前尚不能排除CaV2.1、CaV1.2和K2P1.1通道的潜在作用。
