Induction of CB2 receptor expression in the rat spinal cord of neuropathic but not inflammatory chronic pain models

被引:332
作者
Zhang, J [1 ]
Hoffert, C [1 ]
Vu, HK [1 ]
Groblewski, T [1 ]
Ahmad, S [1 ]
O'Donnell, D [1 ]
机构
[1] AstraZeneca R&D Montreal, Quebec City, PQ H4S 1Z9, Canada
关键词
cannabinoids; inflammation; nerve injury;
D O I
10.1046/j.1460-9568.2003.02704.x
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Cannabinoids have been considered for some time as potent therapeutic agents in chronic pain management. Central and systemic administration of natural, synthetic and endogenous cannabinoids produce antinociceptive and antihyperalgesic effects in both acute and chronic animal pain models. Although much of the existing data suggest that the analgesic effects of cannabinoids are mediated via neuronal CB1 receptors, there is increasing evidence to support a role for peripheral CB2 receptors, which are expressed preferentially on immune cells. As yet, little is known about the central contribution of CB2 in neuropathic pain states. We report here that chronic pain models associated with peripheral nerve injury, but not peripheral inflammation, induce CB2 receptor expression in a highly restricted and specific manner within the lumbar spinal cord. Moreover, the appearance of CB2 expression coincides with the appearance of activated microglia.
引用
收藏
页码:2750 / 2754
页数:5
相关论文
共 29 条
[1]   MICROGLIA EMERGE FROM THE FOG [J].
ALTMAN, J .
TRENDS IN NEUROSCIENCES, 1994, 17 (02) :47-49
[2]   A PERIPHERAL MONONEUROPATHY IN RAT THAT PRODUCES DISORDERS OF PAIN SENSATION LIKE THOSE SEEN IN MAN [J].
BENNETT, GJ ;
XIE, YK .
PAIN, 1988, 33 (01) :87-107
[3]   Cannabinoid receptors and the regulation of immune response [J].
Berdyshev, EV .
CHEMISTRY AND PHYSICS OF LIPIDS, 2000, 108 (1-2) :169-190
[4]   Immunomodulation by cannabinoids is absent in mice deficient for the cannabinoid CB2 receptor [J].
Buckley , NE ;
McCoy, KL ;
Mezey, É ;
Bonner, T ;
Zimmer, A ;
Felder, CC ;
Glass, M ;
Zimmer, A .
EUROPEAN JOURNAL OF PHARMACOLOGY, 2000, 396 (2-3) :141-149
[5]   Control of pain initiation by endogenous cannabinoids [J].
Calignano, A ;
La Rana, G ;
Giuffrida, A ;
Piomelli, D .
NATURE, 1998, 394 (6690) :277-281
[6]   Cloning and characterization of a cDNA encoding a novel subtype of rat thyrotropin-releasing hormone receptor [J].
Cao, J ;
O'Donnell, D ;
Vu, H ;
Payza, K ;
Pou, C ;
Godbout, C ;
Jakob, A ;
Pelletier, M ;
Lembo, P ;
Ahmad, S ;
Walker, P .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (48) :32281-32287
[7]   CB1 and CB2 cannabinoid receptors are implicated in inflammatory pain [J].
Clayton, N ;
Marshall, FH ;
Bountra, C ;
O'Shaughnessy, CT .
PAIN, 2002, 96 (03) :253-260
[8]   Genomic and functional changes induced by the activation of the peripheral cannabinoid receptor CB2 in the promyelocytic cells HL-60 -: Possible involvement of the CB2 receptor in cell differentiation [J].
Derocq, JM ;
Jbilo, O ;
Bouaboula, M ;
Ségui, M ;
Clère, C ;
Casellas, P .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (21) :15621-15628
[9]   Cannabinoid CB1 receptor expression in rat spinal cord [J].
Farquhar-Smith, WP ;
Egertová, M ;
Bradbury, EJ ;
McMahon, SB ;
Rice, ASC ;
Elphick, MR .
MOLECULAR AND CELLULAR NEUROSCIENCE, 2000, 15 (06) :510-521
[10]   The role of central and peripheral Cannabinoid1 receptors in the antihyperalgesic activity of cannabinoids in a model of neuropathic pain [J].
Fox, A ;
Kesingland, A ;
Gentry, C ;
McNair, K ;
Patel, S ;
Urban, L ;
James, I .
PAIN, 2001, 92 (1-2) :91-100