Intraneural dexamethasone applied simultaneously to rat sciatic nerve constriction delays the development of hyperalgesia and allodynia

被引:24
作者
Bastos, Leandro F. S. [1 ,2 ]
Medeiros, Daniel C. [1 ]
Vieira, Rafael P. [3 ]
Watkins, Linda R. [2 ]
Coelho, Marcio M. [4 ]
Moraes, Marcio F. D. [1 ]
机构
[1] Univ Fed Minas Gerais, Inst Ciencias Biol, Dept Fisiol & Biofis, Nucleo Neurociencias NNC, BR-31270901 Belo Horizonte, MG, Brazil
[2] Univ Colorado, Dept Psychol & Neurosci, Boulder, CO 80309 USA
[3] Univ Fed Minas Gerais, Inst Ciencias Exatas, Dept Quim, BR-31270901 Belo Horizonte, MG, Brazil
[4] Univ Fed Minas Gerais, Fac Farm, Dept Prod Farmaceut, Farmacol Lab, BR-31270901 Belo Horizonte, MG, Brazil
关键词
Chronic constriction injury; Neuropathic pain; Peripheral neuropathy; Inflammation; Neuroimmune interaction; Corticosteroid; DORSAL-ROOT GANGLIA; NEUROPATHIC PAIN; THERMAL HYPERALGESIA; EXPRESSION; GLUCOCORTICOIDS; IMMUNE; INJURY; NOCICEPTION; NEURONS; CELLS;
D O I
10.1016/j.neulet.2011.12.062
中图分类号
Q189 [神经科学];
学科分类号
071006 [神经生物学];
摘要
Although neuroimmune interactions associated with the development of pain sensitization in models of neuropathic pain have been widely studied, there are some aspects that require further investigation. Thus, we aimed to evaluate whether the local intraneural or perineural injections of dexamethasone, an efficacious anti-inflammatory and immunosuppressant drug, delays the development of both thermal hyperalgesia and mechanical allodynia in an experimental model of neuropathic pain in rats. Hargreaves and electronic von Frey tests were applied. The chronic constriction injury (CCI) of right sciatic nerve was performed. Single intraneural dexamethasone administration at the moment of constriction delayed the development of sensitization for thermal hyperalgesia and mechanical allodynia. However, perineural administration of dexamethasone, at the highest dose, did not delay experimental pain development. These results show that inflammation/immune response at the site of nerve lesion is an essential trigger for the pathological changes that lead to both hyperalgesia and allodynia. In conclusion, this approach opens new opportunities to study cellular and molecular neuroimmune interactions associated with the development of pain derived from peripheral neuropathies. (C) 2012 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:20 / 23
页数:4
相关论文
共 28 条
[1]
Corticosteroid effects on cell signalling [J].
Barnes, PJ .
EUROPEAN RESPIRATORY JOURNAL, 2006, 27 (02) :413-426
[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]
ROLE OF PERI-AXONAL INFLAMMATION IN THE DEVELOPMENT OF THERMAL HYPERALGESIA AND GUARDING BEHAVIOR IN A RAT MODEL OF NEUROPATHIC PAIN [J].
CLATWORTHY, AL ;
ILLICH, PA ;
CASTRO, GA ;
WALTERS, ET .
NEUROSCIENCE LETTERS, 1995, 184 (01) :5-8
[4]
Costigan M., 2009, ANN REV NEUROSCI
[5]
Inhibition of Th1 immune response by glucocorticoids, dexamethasone selectively inhibits IL-12-induced Stat4 phosphorylation in T lymphocytes [J].
Franchimont, D ;
Galon, J ;
Gadina, M ;
Visconti, R ;
Zhou, YJ ;
Aringer, M ;
Frucht, DM ;
Chrousos, GP ;
O'Shea, JJ .
JOURNAL OF IMMUNOLOGY, 2000, 164 (04) :1768-1774
[6]
Transgenic inhibition of glial NF-kappa B reduces pain behavior and inflammation after peripheral nerve injury [J].
Fu, Eugene S. ;
Zhang, Yan Ping ;
Sagen, Jacqueline ;
Candiotti, Keith A. ;
Morton, Paul D. ;
Liebl, Daniel J. ;
Bethea, John R. ;
Brambilla, Roberta .
PAIN, 2010, 148 (03) :509-518
[7]
THERMAL BIOLOGY OF THE LABORATORY RAT [J].
GORDON, CJ .
PHYSIOLOGY & BEHAVIOR, 1990, 47 (05) :963-991
[8]
A NEW AND SENSITIVE METHOD FOR MEASURING THERMAL NOCICEPTION IN CUTANEOUS HYPERALGESIA [J].
HARGREAVES, K ;
DUBNER, R ;
BROWN, F ;
FLORES, C ;
JORIS, J .
PAIN, 1988, 32 (01) :77-88
[9]
Effect of local methylprednisolone on pain in a nerve injury model - A pilot study [J].
Johansson, A ;
Bennett, GJ .
REGIONAL ANESTHESIA, 1997, 22 (01) :59-65
[10]
Regulation of bronchoalveolar macrophage proinflammatory cytokine production by dexamethasone and granulocyte-macrophage colony-stimulating factor after stimulation by Aspergillus conidia or lipopolysaccharide [J].
Kamberi, M ;
Brummer, E ;
Stevens, DA .
CYTOKINE, 2002, 19 (01) :14-20