Division of Oral Physiology, Department of Oral Biological Science, Niigata University Graduate School of Medical and Dental Sciences, 2-5274, Gakkocho-dori, Niigata, 951-8514, Japan.
Eur J Neurosci. 2014 Jun;39(12):2050-9. doi: 10.1111/ejn.12562. Epub 2014 Mar 25.
To evaluate the mechanisms underlying orofacial motor dysfunction associated with trigeminal nerve injury, we studied the astroglial cell activation following chronic constriction injury (CCI) of the infraorbital nerve (ION) immunohistochemically, nocifensive behavior in ION-CCI rats, and the effect of the glutamine synthase (GS) blocker methionine sulfoximine (MSO) on the jaw-opening reflex (JOR), and also studied whether glutamate-glutamine shuttle mechanism is involved in orofacial motor dysfunction. GFAP-immunoreactive (IR) cells were observed in the trigeminal motor nucleus (motV) 3 and 14 days after ION-CCI, and the nocifensive behavior and JOR amplitude were also strongly enhanced at these times. The number of GS- and GFAP-IR cells was also significantly higher in ION-CCI rats on day 7. The amplitude and duration of the JOR were strongly suppressed after MSO microinjection (m.i.) into the motV compared with that before MSO administration in ION-CCI rats. After MSO administration, the JOR amplitude was strongly suppressed, and the duration of the JOR was shortened. Forty minutes after m.i. of glutamine, the JOR amplitude was gradually returned to the control level and the strongest attenuation of the suppressive effect of MSO was observed at 180 min after glutamine m.i. In addition, glutamine also attenuated the MSO effect on the JOR duration, and the JOR duration was extended and returned to the control level thereafter. The present findings suggest that astroglial glutamate-glutamine shuttle in the motV is involved in the modulation of excitability of the trigeminal motoneurons affecting the enhancement of various jaw reflexes associated with trigeminal nerve injury.
为了评估与三叉神经损伤相关的口面运动功能障碍的机制，我们通过免疫组织化学方法研究了眶下神经（ION）慢性缩窄性损伤（CCI）后星形胶质细胞的激活，ION-CCI 大鼠的伤害性行为，以及谷氨酰胺合成酶（GS）抑制剂甲硫氨酸亚砜（MSO）对张口反射（JOR）的影响，还研究了谷氨酸-谷氨酰胺穿梭机制是否参与口面运动功能障碍。在 ION-CCI 后 3 天和 14 天观察到三叉神经运动核（motV）中 GFAP-免疫反应（IR）细胞，并且此时伤害性行为和 JOR 幅度也强烈增强。在 ION-CCI 大鼠中，第 7 天 GS 和 GFAP-IR 细胞的数量也显著增加。与 MSO 给药前相比，MSO 微量注射（m.i.）到 motV 后 JOR 的幅度和持续时间均强烈抑制。MSO 给药后，JOR 幅度强烈抑制，JOR 持续时间缩短。在 m.i. 谷氨酰胺 40 分钟后，JOR 幅度逐渐恢复到对照水平，并且在 m.i. 谷氨酰胺 180 分钟后观察到 MSO 抑制作用的最强衰减。此外，谷氨酰胺还减弱了 MSO 对 JOR 持续时间的作用，并且 JOR 持续时间延长并随后恢复到对照水平。这些发现表明，motV 中的星形胶质细胞谷氨酸-谷氨酰胺穿梭参与调节三叉神经运动神经元的兴奋性，从而影响与三叉神经损伤相关的各种口颌反射的增强。
