Chemokines, neuronal-glial interactions, and central processing of neuropathic pain.
Chemokines, neuronal-glial interactions, and central processing of neuropathic pain.
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DOI：
10.1016/j.pharmthera.2010.01.002
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发表时间：
2010-04
影响因子：
13.5
通讯作者：
Ji, Ru-Rong
中科院分区：
文献类型：
--
作者：
Gao, Yong-Jing;Ji, Ru-Rong
全世界数以百万计的人因各种疾病条件下神经系统的损伤或功能障碍而遭受神经性疼痛。发展有效的治疗策略需要更好地了解神经病理性疼痛发病的分子和细胞机制。越来越多的人认识到，小胶质细胞和星形胶质细胞等脊髓胶质细胞通过释放促炎细胞因子和趋化因子等强大的神经调节剂，在神经病理性疼痛的诱导和维持中发挥关键作用。最近的证据表明，趋化因子是疼痛控制的新参与者。在本文中，我们综述了趋化因子通过神经元-神经胶质相互作用调节疼痛的证据，重点介绍了两种趋化因子CX3CL1(Fractalkine)和CCL2(MCP-1)的中心作用，因为它们对神经元-神经胶质相互作用有不同的调节作用。从神经元释放CX3CL1是介导神经元到小胶质细胞信号转导的理想途径，因为这种趋化因子的唯一受体CX3CR1在脊髓小胶质细胞中表达，该受体的激活导致小胶质细胞中p38 MAP激酶的磷酸化。虽然CCL2参与了神经元到小胶质细胞的信号转导，但最近的一项研究表明，CCL2在神经损伤后星形胶质细胞到神经元的信号转导中发挥了新的作用。特别是，CCL2通过增加背角神经元中NMDA受体的活性而迅速诱导中枢敏化。深入了解神经损伤后趋化因子在神经元-神经胶质细胞相互作用中的作用，将为神经病理性疼痛的治疗干预确定新的靶点。
Millions of people worldwide suffer from neuropathic pain as a result of damage to or dysfunction of the nervous system under various disease conditions. Development of effective therapeutic strategies requires a better understanding of molecular and cellular mechanisms underlying the pathogenesis of neuropathic pain. It has been increasingly recognized that spinal cord glial cells such as microglia and astrocytes play a critical role in the induction and maintenance of neuropathic pain by releasing powerful neuromodulators such as proinflammatory cytokines and chemokines. Recent evidence reveals chemokines as new players in pain control. In this article, we review evidence for chemokine modulation of pain via neuronal-glial interactions by focusing on the central role of two chemokines, CX3CL1 (fractalkine) and CCL2 (MCP-1), because they differentially regulate neuronal-glial interactions. Release of CX3CL1 from neurons is ideal to mediate neuronal-to-microglial signaling, since the sole receptor of this chemokine, CX3CR1, is expressed in spinal microglia and activation of the receptor leads to phosphorylation of p38 MAP kinase in microglia. Although CCL2 was implicated in neuronal-to-microglial signaling, a recent study shows a novel role of CCL2 in astroglial-to-neuronal signaling after nerve injury. In particular, CCL2 rapidly induces central sensitization by increasing the activity of NMDA receptors in dorsal horn neurons. Insights into the role of chemokines in neuronal-glial interactions after nerve injury will identify new targets for therapeutic intervention of neuropathic pain.
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影响因子：
5.3
作者：
Bourd-Boittin K;Basset L;Bonnier D;L'helgoualc'h A;Samson M;Théret N
通讯作者：
Théret N
DOI：
10.1523/jneurosci.3295-09.2010
发表时间：
2010-01-13
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Clark AK;Staniland AA;Marchand F;Kaan TK;McMahon SB;Malcangio M
通讯作者：
Malcangio M
影响因子：
3.3
作者：
Bhangoo SK;Ripsch MS;Buchanan DJ;Miller RJ;White FA
通讯作者：
White FA
影响因子：
4.7
作者：
Bertollini, Cristina;Ragozzino, Davide;Eusebi, Fabrizio
通讯作者：
Eusebi, Fabrizio
影响因子：
4.7
作者：
Bajetto, A;Bonavia, R;Schettini, G
通讯作者：
Schettini, G