Takeda M, Tanimoto T, Ikeda M, Nasu M, Kadoi J, Yoshida S, Matsumoto S
Department of Physiology, School of Dentistry at Tokyo, Nippon Dental University, 1-9-20, Fujimi-cho, Chiyoda-ku, Tokyo 102-8159, Japan.
Neuroscience. 2006;138(2):621-30. doi: 10.1016/j.neuroscience.2005.11.024. Epub 2006 Jan 4.
The aim of the present study was to investigate the effect of temporomandibular joint inflammation on the excitability of trigeminal root ganglion neurons innervating the temporomandibular joint using a perforated patch-clamp technique. Inflammation was induced by injection of complete Freund's adjuvant into the rat temporomandibular joint. The threshold for escape from mechanical stimulation in the temporomandibular joint-inflamed rats was significantly lower than that in control rats. Fluorogold labeling was used to identify the trigeminal root ganglion neurons innervating the site of inflammation. When voltage-clamp (V(h)=-60 mV) conditions were applied to these Fluorogold-labeled small diameter trigeminal root ganglion neurons (<30 mum), voltage-dependent transient K(+) current densities were significantly reduced in the inflamed rats compared with controls. In addition, the voltage-dependence of inactivation of the voltage-dependent transient K(+) current was negatively shifted in the labeled temporomandibular joint-inflamed trigeminal root ganglion neurons. Furthermore, temporomandibular joint inflammation significantly reduced the threshold current and significantly increased action potential firings evoked at two-fold threshold in the Fluorogold-labeled small trigeminal root ganglion neurons. Application of 4-aminopyridine (0.5mM) to control trigeminal root ganglion neurons mimicked the changes in the firing properties observed after complete Freund's adjuvant treatment. Together, these results suggest that temporomandibular joint inflammation increases the excitability of trigeminal root ganglion neurons innervating temporomandibular joint by suppressing voltage-dependent transient K(+) current via a leftward shift in the inactivation curve. These changes may contribute to trigeminal inflammatory allodynia in temporomandibular joint disorder.
本研究的目的是使用穿孔膜片钳技术，研究颞下颌关节炎症对支配颞下颌关节的三叉神经根节神经元兴奋性的影响。通过向大鼠颞下颌关节注射完全弗氏佐剂诱导炎症。颞下颌关节炎症大鼠逃避机械刺激的阈值显著低于对照大鼠。使用荧光金标记来识别支配炎症部位的三叉神经根节神经元。当对这些荧光金标记的小直径三叉神经根节神经元（<30μm）施加电压钳（V（h）=-60mV）条件时，与对照相比，炎症大鼠的电压依赖性瞬时K（+）电流密度显著降低。此外，在标记的颞下颌关节炎症三叉神经根节神经元中，电压依赖性瞬时K（+）电流失活的电压依赖性负向偏移。此外，颞下颌关节炎症显著降低了阈值电流，并显著增加了荧光金标记的小三叉神经根节神经元在两倍阈值时诱发的动作电位发放。将4-氨基吡啶（0.5mM）应用于对照三叉神经根节神经元可模拟完全弗氏佐剂处理后观察到的放电特性变化。总之，这些结果表明，颞下颌关节炎症通过使失活曲线向左移位来抑制电压依赖性瞬时K（+）电流，从而增加支配颞下颌关节的三叉神经根节神经元的兴奋性。这些变化可能导致颞下颌关节紊乱中的三叉神经炎性痛觉过敏。
