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首页> 外文期刊>Molecular pain >Involvement of peripheral ionotropic glutamate receptors in orofacial thermal hyperalgesia in rats
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Involvement of peripheral ionotropic glutamate receptors in orofacial thermal hyperalgesia in rats

机译：周围离子型谷氨酸受体在大鼠口面部热痛觉过敏中的作用

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Background The purpose of the present study was to elucidate the mechanisms that may underlie the sensitization of trigeminal spinal subnucleus caudalis (Vc) and upper cervical spinal cord (C1-C2) neurons to heat or cold stimulation of the orofacial region following glutamate (Glu) injection. Results Glu application to the tongue or whisker pad skin caused an enhancement of head-withdrawal reflex and extracellular signal-regulated kinase (ERK) phosphorylation in Vc-C2 neurons. Head-withdrawal reflex and ERK phosphorylation were also enhanced following cold stimulation of the tongue but not whisker pad skin in Glu-injected rats, and the head-withdrawal reflex and ERK phosphorylation were enhanced following heat stimulation of the tongue or whisker pad skin. The enhanced head-withdrawal reflex and ERK phosphorylation after heat stimulation of the tongue or whisker pad skin, and those following cold stimulation of the tongue but not whisker pad skin were suppressed following ionotropic glutamate receptor antagonists administration into the tongue or whisker pad skin. Furthermore, intrathecal administration of MEK1/2 inhibitor PD98059 caused significant suppression of enhanced head-withdrawal reflex in Glu-injected rats, heat head-withdrawal reflex in the rats with Glu injection into the tongue or whisker pad skin and cold head-withdrawal reflex in the rats with Glu injection into the tongue. Conclusions The present findings suggest that peripheral Glu receptor mechanisms may contribute to cold hyperalgesia in the tongue but not in the facial skin, and also contribute to heat hyperalgesia in the tongue and facial skin, and that the mitogen-activated protein kinase cascade in Vc-C2 neurons may be involved in these Glu-evoked hyperalgesic effects.
机译：背景技术本研究的目的是阐明可能是谷氨酸（Glu）后三叉神经脊髓尾核（Vc）和上颈脊髓（C1-C2）神经元对口面区域进行热或冷刺激的敏感性的机制。注射。结果Glu在舌头或晶须皮肤上的应用导致Vc-C2神经元的退缩反射和细胞外信号调节激酶（ERK）磷酸化增强。冷刺激舌头，但不刺激晶须垫皮肤的人，退缩反射和ERK磷酸化也增强，而舌头或晶须皮肤的热刺激后，退缩反射和ERK磷酸化也增强。在舌头或晶须皮中使用离子型谷氨酸受体拮抗剂后，对舌头或晶须皮进行热刺激后，以及对舌头进行冷刺激而不是晶须皮后增强的退缩反射和ERK磷酸化得到抑制。此外，鞘内注射MEK1 / 2抑制剂PD98059可显着抑制注射Glu的大鼠的退缩反射增强，将Glu注射至舌头或晶须皮肤的大鼠的退热反射和抑制退热的退缩。用谷氨酸注射入大鼠的舌头。结论目前的发现表明，外周Glu受体机制可能有助于舌头而非面部皮肤的冷痛觉过敏，并且还有助于舌头和面部皮肤的热痛觉过敏，并且促细胞分裂素激活的蛋白激酶在Vc- C2神经元可能参与了这些由Glu引起的痛觉过敏作用。

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