Nitric oxide‐induced increase of excitatory amino acid levels in the trigeminal nucleus caudalis of the rat with tactile hypersensitivity evoked by the loose‐ligation of the inferior alveolar nerves
Nitric oxide‐induced increase of excitatory amino acid levels in the trigeminal nucleus caudalis of the rat with tactile hypersensitivity evoked by the loose‐ligation of the inferior alveolar nerves
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DOI：
10.1111/j.1471-4159.2004.02768.x
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发表时间：
2004-11
影响因子：
4.7
通讯作者：
Toyohiro Fujita;Y. Kamisaki;N. Yonehara
中科院分区：
文献类型：
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作者：
Toyohiro Fujita;Y. Kamisaki;N. Yonehara
为了研究三叉神经系统中N -甲基- d -天门氨酸(NMDA)/一氧化氮（NO）通路是否参与了牙科手术后痛觉过敏和异位性疼痛等病理性疼痛状态的发生和/或维持，我们通过体内微透析检测了脑干三叉神经感觉核复合体（SpVc - I，II）尾侧亚核浅层兴奋性氨基酸（EAA）水平的改变模式。与假手术大鼠相比，结扎动物在灌流开始后立即观察到非常高的EAA释放反应。结扎组与假手术组相比，应用40 - V牙髓刺激或1%辣椒素乳膏诱发的EAA水平显著升高。在灌注液中加入100µm的羧基- PTIO可抑制辣椒素乳膏诱导的EAA水平升高。在结扎动物和假手术动物的灌注液中应用SNAP （2mm）可提高eaa水平。然而，与假手术动物相比，结扎动物中SNAP诱发的EAA水平无显著差异。这些结果表明，刺激引起的EAA水平升高发生在牙痛通路的第一突触中继部位，并通过内源性NO表达，在牙周围神经损伤后病理疼痛状态的发展和/或维持中起重要作用。
To investigate whether or not N‐methyl‐d‐aspartate (NMDA)/nitric oxide (NO) pathway in the trigeminal system is involved in the development and/or maintenance of such pathological pain states as the hyperalgesia and allodynia observed after dental surgery, we examined the alteration patterns of excitatory amino acid (EAA) level in the superficial layer of subnucleus caudalis of the brain‐stem trigeminal sensory nuclear complex (SpVc‐I,II) by in vivo microdialysis. A very high EAA release response was observed immediately after the start of the perfusion in ligated animals compared with sham‐operated rats. The EAA level evoked by application of the 40‐V tooth pulp‐stimulation or 1% capsaicin cream was significantly higher in the ligated animals than those in the sham‐operated animals. This increase of EAA level induced by capsaicin cream was inhibited by adding carboxy‐PTIO (100 µm) to the perfusate. The applications of SNAP (2 mm) into the perfusate enhanced the level of EAAs in ligated animals and sham‐operated animals. However, SNAP‐evoked EAA levels in ligated animals were not significantly different compared with those of sham‐operated animals. These results suggest that alterations in the stimulus‐evoked raised EAA levels that occur in the site of the first synaptic relay of the dental pain pathway and which are expressed via endogenous NO, and which play an important role in development and/or maintenance of pathological pain states following dental peripheral nerve injury.