Flake Natasha M, Gold Michael S
Department of Biomedical Sciences, Dental School, University of Maryland, 666 W. Baltimore St., Room 5-A-12, Baltimore, MD 21201, USA.
Neurosci Lett. 2005 Aug 26;384(3):294-9. doi: 10.1016/j.neulet.2005.04.091.
Inflammation-induced changes in voltage-gated sodium currents (I(Na)) in primary afferent neurons may contribute to hyperexcitability and pain. The present study was designed to test the hypothesis that persistent inflammation of the temporomandibular joint (TMJ) increases I(Na) in TMJ afferents. Acutely dissociated retrogradely labeled TMJ afferents were studied using whole-cell patch clamp techniques three days following Complete Freund's Adjuvant-induced inflammation of the TMJ. Inflammation was associated with a decrease in tetrodotoxin (TTX)-sensitive Na+ conductance and no significant change in slowly inactivating TTX-resistant Na+ conductance. However, inflammation increased the excitability of TMJ afferents. These results suggest that changes in ion channels other than those underlying TTX-sensitive and the slowly inactivating TTX-resistant Na+ conductance are likely to account for the inflammation-induced increase in the excitability of TMJ afferents.
炎症诱导的初级传入神经元电压门控钠电流（I(Na)）变化可能导致兴奋性过高和疼痛。本研究旨在验证颞下颌关节（TMJ）持续性炎症会增加TMJ传入神经I(Na)这一假说。在完全弗氏佐剂诱导TMJ炎症三天后，使用全细胞膜片钳技术对急性解离的逆行标记TMJ传入神经进行研究。炎症与河豚毒素（TTX）敏感的Na+电导降低以及缓慢失活的TTX抗性Na+电导无显著变化有关。然而，炎症增加了TMJ传入神经的兴奋性。这些结果表明，除了TTX敏感和缓慢失活的TTX抗性Na+电导所涉及的离子通道变化外，其他离子通道变化可能是炎症诱导TMJ传入神经兴奋性增加的原因。
