Studies of the mechanism and discovery of animal model in neuropathic pain

疼痛控制非常重要。疼痛的机制尚未完全了解。因此，我们研究神经病理性疼痛的机制和发现神经病理性疼痛在中枢神经系统。(1)我们研究了趋化因子，趋化细胞因子配体-1（CCL-1）在神经病理性疼痛中的功能作用。在脊髓中预先施用抗CCL-1抗体抑制异常性疼痛。这一结果支持脊髓CCL-1有助于神经病理性疼痛的发展。(2)我们证明了大脑中的毒蕈碱受体如何参与神经病理性疼痛。激活扣带回M1受体可减轻神经病理性疼痛，其镇痛作用是通过激活GABA能神经元介导的。(3)胆碱酯酶抑制剂多奈哌齐和加兰他敏通过中枢毒蕈碱受体减少神经性疼痛模型中的痛觉过敏。多奈哌齐和加兰他敏可能有助于神经病理性疼痛的治疗结果。

Pain control is very important. The mechanism of pain is not fully understood. Therefore, we examined the mechanisms of neuropathic pain and the discovery to neuropathic pain in the central nervous system.(1) We examined the functional role of chemokines, chemotactic cytokine ligand-1(CCL-1)in neuropathic pain. Pre-administrations of anti-CCL-1 antibody in the spinal cord inhibited the allodynia. This result supports that spinal CCL-1 contributes to the development of neuropathic pain. (2) We demonstrated how the muscarinic receptors in the brain involve in neuropathic pain. Activation of muscarinic M1 receptors in the the cinglate cortex attenuated the neuropathic pain and the analgesic effect was mediated by activation of GABAergic neuron. (3) Cholinesterase inhibitor donepezil and galantamine reduced hyperalgesia via central muscarinic receptors in the neuropathic pain model. Donepezil and galantamine may be useful in the therapeutic outcome in the management of neuropathic pain.