p38 MAPK, microglial signaling, and neuropathic pain

被引：489

作者：

Ji, Ru-Rong ^{[1
,2
]}

Suter, Marc R. ^{[1
,2
]}

机构：

[1] Brigham & Womens Hosp, Dept Anesthesiol, Pain Res Ctr, Boston, MA 02115 USA

[2] Harvard Med Sch, Boston, MA USA

来源：

MOLECULAR PAIN | 2007年 / 3卷

关键词：

D O I：

10.1186/1744-8069-3-33

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Accumulating evidence over last several years indicates an important role of microglial cells in the pathogenesis of neuropathic pain. Signal transduction in microglia under chronic pain states has begun to be revealed. We will review the evidence that p38 MAPK is activated in spinal microglia after nerve injury and contributes importantly to neuropathic pain development and maintenance. We will discuss the upstream mechanisms causing p38 activation in spinal microglia after nerve injury. We will also discuss the downstream mechanisms by which p38 produces inflammatory mediators. Taken together, current data suggest that p38 plays a critical role in microglial signaling under neuropathic pain conditions and represents a valuable therapeutic target for neuropathic pain management.

引用

页数：9

共 68 条

[1] Impaired neuropathic pain responses in mice lacking the chemokine receptor CCR2 [J].

Abbadie, C ;

Lindia, JA ;

Cumiskey, AM ;

Peterson, LB ;

Mudgett, JS ;

Bayne, EK ;

DeMartino, JA ;

MacIntyre, DE ;

Forrest, MJ .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (13) :7947-7952

[2]

Bhat NR, 1998, J NEUROSCI, V18, P1633

[3] Regulation of peripheral inflammation by spinal p38 MAP kinase in rats [J].

Boyle, David L. ;

Jones, Toni L. ;

Hammaker, Deepa ;

Svensson, Camille I. ;

Rosengren, Sanna ;

Albani, Salvatore ;

Sorkin, Linda ;

Firestein, Gary S. .

PLOS MEDICINE, 2006, 3 (09) :1616-1624

[4]

CLARK AK, 2007, P NATL ACAD SCI US

[5] Rapid co-release of interleukin 1β and caspase 1 in spinal cord inflammation [J].

Clark, Anna K. ;

D'Aquisto, Fulvio ;

Gentry, Clive ;

Marchand, Fabien ;

McMahon, Stephen B. ;

Malcangio, Marzia .

JOURNAL OF NEUROCHEMISTRY, 2006, 99 (03) :868-880

[6] Dissociation of microglial activation and neuropathic pain behaviors following peripheral nerve injury in the rat [J].

Colburn, RW ;

DeLeo, JA ;

Rickman, AJ ;

Yeager, MP ;

Kwon, P ;

Hickey, WF .

JOURNAL OF NEUROIMMUNOLOGY, 1997, 79 (02) :163-175

[7] BDNF from microglia causes the shift in neuronal anion gradient underlying neuropathic pain [J].

Coull, JAM ;

Beggs, S ;

Boudreau, D ;

Boivin, D ;

Tsuda, M ;

Inoue, K ;

Gravel, C ;

Salter, MW ;

De Koninck, Y .

NATURE, 2005, 438 (7070) :1017-1021

[8] Trans-synaptic shift in anion gradient in spinal lamina I neurons as a mechanism of neuropathic pain [J].

Coull, JAM ;

Boudreau, D ;

Bachand, K ;

Prescott, SA ;

Nault, F ;

Sik, A ;

De Koninck, P ;

De Koninck, Y .

NATURE, 2003, 424 (6951) :938-942

[9] Activation of p38 mitogen-activated protein kinase in spinal microglia mediates morphine antinociceptive tolerance [J].

Cui, Y ;

Chen, Y ;

Zhi, JL ;

Guo, RX ;

Feng, JQ ;

Chen, PX .

BRAIN RESEARCH, 2006, 1069 (01) :235-243

[10] The role of neuroinflammation and neuroimmune activation in persistent pain [J].

DeLeo, JA ;

Yezierski, RP .

PAIN, 2001, 90 (1-2) :1-6

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