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首页> 外文期刊>Neuroscience Letters: An International Multidisciplinary Journal Devoted to the Rapid Publication of Basic Research in the Brain Sciences >Intracellular messengers involved in spontaneous pain, heat hyperalgesia, and mechanical allodynia induced by intrathecal dihydroxyphenylglycine.
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Intracellular messengers involved in spontaneous pain, heat hyperalgesia, and mechanical allodynia induced by intrathecal dihydroxyphenylglycine.

机译：鞘内二羟基苯基甘氨酸引起的自发性疼痛，热痛觉过敏和机械性异常性疼痛的细胞内信使。

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摘要

We investigated the role of two intracellular second messengers, extracellular signal-regulated protein kinase (ERK) and protein kinase C (PKC), in a model of persistent pain using intrathecal (i.t.) (R,S)-3,5-dihydroxyphenylglycine (DHPG). Spontaneous nociceptive behaviours (SNBs), mechanical allodynia (von Frey thresholds) and heat hyperalgesia (plantar test latencies) induced by DHPG were measured in animals pretreated i.t. with membrane permeable inhibitors of ERK (PD 98059) and PKC (GF 109203X). Spinal administration of PD 98059 dose-dependently reduced SNBs, and attenuated both mechanical allodynia and heat hyperalgesia induced by DHPG. GF 109203X treatment also reduced SNBs and heat hyperalgesia, but did not affect mechanical allodynia induced by DHPG. Neither PD 98059, nor GF 109203X, altered mechanical or thermal thresholds in saline-injected control rats. These results suggest that both ERK and PKC are involved in persistent pain associated with the i.t. administration of DHPG.
机译：我们在使用鞘内（it）（R，S）-3,5-dihydroxyphenylglycine（）的持续性疼痛模型中研究了两个细胞内第二信使，细胞外信号调节蛋白激酶（ERK）和蛋白激酶C（PKC）的作用。 DHPG）。在经i.t.预处理的动物中测量了DHPG诱导的自发伤害行为（SNB），机械性异常性疼痛（von Frey阈值）和热痛觉过敏（足底测试潜伏期）。使用ERK（PD 98059）和PKC（GF 109203X）的膜渗透抑制剂。脊髓给药PD 98059剂量依赖性地减少了SNB，并减弱了DHPG诱导的机械性异常性疼痛和热痛觉过敏。 GF 109203X处理还减少了SNB和热痛觉过敏，但不影响DHPG引起的机械性异常性疼痛。 PD 98059和GF 109203X均未改变注射盐水的对照组的机械或热阈值。这些结果表明，ERK和PKC都参与了与i.t.相关的持续性疼痛。 DHPG的管理。

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