Inflammation alters sodium currents and excitability of temporomandibular joint afferents
Inflammation alters sodium currents and excitability of temporomandibular joint afferents
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DOI：
10.1016/j.neulet.2005.04.091
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发表时间：
2005-08-26
影响因子：
2.5
通讯作者：
Gold, MS
中科院分区：
文献类型：
--
作者：
Flake, NM;Gold, MS
炎症诱导的初级传入神经元电压门控钠电流（I-Na）的变化可能导致过度兴奋和疼痛。本研究旨在验证颞下颌关节（TMJ）持续炎症增加TMJ传入的I-Na的假设。急性解离逆行标记颞下颌关节的传入进行了研究，使用全细胞膜片钳技术三天后完全弗氏佐剂诱导的炎症颞下颌关节。炎症与河豚毒素（TTX）敏感的Na+电导的降低相关，而缓慢灭活TTX抗性Na+电导无显著变化。然而，炎症增加颞下颌关节传入的兴奋性。这些结果表明，离子通道的变化比那些潜在的TTX敏感和缓慢失活TTX抗性Na+电导可能占炎症引起的兴奋性增加TMJ传入。(c)2005爱思唯尔爱尔兰有限公司保留所有权利。
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. (c) 2005 Elsevier Ireland Ltd. All rights reserved.