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首页> 外文期刊>The European Journal of Neuroscience >Ca/calmodulin-dependent protein kinase II in the spinal cord contributes to neuropathic pain in a rat model of mononeuropathy.
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Ca/calmodulin-dependent protein kinase II in the spinal cord contributes to neuropathic pain in a rat model of mononeuropathy.

机译：脊髓中Ca /钙调蛋白依赖性蛋白激酶II导致单神经病大鼠模型的神经性疼痛。

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Abstract Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) is known to subserve activity-dependent neuronal plasticity in the central nervous system. To examine in vivo the implication of spinal CaMKII activity in the generation and development of neuropathic pain after peripheral nerve injury, we used an animal model of mononeuropathy, the chronic constriction injury (CCI) model, in the rat. We found that, 3 days after CCI, the total CaMKII (tCaMKII) immunoreactivity increased in the superficial laminae of the spinal cord and this increase continued for up to 14 days. The immunoreactivity of phosphorylated CaMKII showed an increase from 1 day after CCI, which preceded the up-regulation of tCaMKII. A non-selective N-methyl-d-aspartate receptor antagonist, MK801, significantly attenuated the increase of tCaMKII and phosphorylated CaMKII. Moreover, intrathecal administration of an inhibitor of CaMKII, KN93, before the CCI surgery attenuated the development of thermal hyperalgesia and mechanical allodynia. In addition, KN93 significantly reduced the nociceptive behavior in phase II of the formalin test. These findings demonstrate that the activity of CaMKII in spinal neurons is elevated after peripheral nerve injury and may be involved in central sensitization. The alteration of CaMKII is considered to be a neuroplastic change that occurs in spinal neurons that contributes to neuropathic pain, suggesting the potential for the development of novel therapeutics for neuropathic pain that target CaMKII.
机译：摘要已知Ca（2 +）/钙调蛋白依赖性蛋白激酶II（CaMKII）在中枢神经系统中具有活动依赖性神经元可塑性。为了在体内检查脊髓CaMKII活性在周围神经损伤后神经性疼痛的产生和发展中的意义，我们在大鼠中使用了单神经病的动物模型，即慢性收缩损伤（CCI）模型。我们发现，CCI后3天，脊髓表层的总CaMKII（tCaMKII）免疫反应性增加，并且这种增加持续了多达14天。磷酸化的CaMKII的免疫反应性从CCI后1天开始增加，这是在tCaMKII上调之前。非选择性的N-甲基-d-天冬氨酸受体拮抗剂MK801，显着减弱了tCaMKII和磷酸化的CaMKII的增加。此外，在CCI手术前鞘内注射CaMKII抑制剂KN93可减轻热痛觉过敏和机械性异常性疼痛的发生。此外，KN93在福尔马林试验的II期显着降低了伤害性行为。这些发现表明，脊髓神经元中CaMKII的活性在周围神经损伤后升高，并且可能参与中枢敏化。 CaMKII的变化被认为是在脊髓神经元中发生的神经塑性变化，有助于神经性疼痛，这表明开发针对CaMKII的神经性疼痛新疗法的潜力。

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