Minocycline treatment reduces white matter damage after excitotoxic striatal injury

被引：35

作者：

Guimaraes, Joanilson S. ^{[2
]}

Freire, Marco Aurelio M. ^{[3
]}

Lima, Rafael R.

Picanco-Diniz, Cristovam W. ^{[3
]}

Pereira, Antonio ^{[2
,4
]}

Gomes-Leal, Walace ^{[1
]}

机构：

[1] Fed Univ Para, Inst Biol Sci, Lab Expt Neuroprotect & Neuroregenerat, BR-66075900 Belem, Para, Brazil

[2] Edmond & Lily Safra Int Inst Neurosci Natal, Natal, RN, Brazil

[3] Fed Univ Para, Inst Biol Sci, Lab Neurodegenerat & Infect, BR-66075900 Belem, Para, Brazil

[4] Univ Fed Rio Grande do Norte, BR-59072970 Natal, RN, Brazil

来源：

BRAIN RESEARCH | 2010年 / 1329卷

关键词：

Excitotoxicity; Neurodegeneration; Oligodendrocyte; Myelin; White matter; Striatum; FOCAL CEREBRAL-ISCHEMIA; SPINAL-CORD-INJURY; INFLAMMATORY RESPONSE; AXONAL DAMAGE; MYELIN IMPAIRMENT; MICROGLIA; RAT; OLIGODENDROCYTES; ACTIVATION; APOPTOSIS;

D O I：

10.1016/j.brainres.2010.03.007

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

We investigated the protective effects of minocycline following white matter damage (WMD) in the rat striatum. Excitotoxic lesions were induced by N-Methyl-D-Aspartate (NMDA) microinjections and caused striatal damage, concomitant with microglial/macrophage activation. The excitotoxic lesion both damaged oligodendrocytes (Tau-1(+) cells) and caused a decrease in tissue reactivity for myelin basic protein (MBP) after post-lesional day 3 (PLD). Treatment with the semi-synthetic tetracycline antibiotic minocycline, however, led to oligodendrocyte preservation and decreased myelin impairment. Taken together, these results suggest that white matter damage (WMD) is an important component of the physiopathology of acute striatal damage and that microglia/macrophage activation contributes to this pathological phenomenon. (C) 2010 Elsevier B.V. All rights reserved.

引用

页码：182 / 193

页数：12

共 51 条

[1] Testing NMDA receptor block as a therapeutic strategy for reducing ischaemic damage to CNS white matter [J].

Bakiri, Yamina ;

Hamilton, Nicola B. ;

Karadottir, Ragnhildur ;

Attwell, David .

GLIA, 2008, 56 (02) :233-240

[2] Review of current evidence for apoptosis after spinal cord injury [J].

Beattie, MS ;

Farooqui, AA ;

Bresnahan, JC .

JOURNAL OF NEUROTRAUMA, 2000, 17 (10) :915-925

[3] EFFECTS OF SILICA ON THE OUTCOME FROM EXPERIMENTAL SPINAL-INJURY - IMPLICATION OF MACROPHAGES IN SECONDARY TISSUE-DAMAGE [J].

BLIGHT, AR .

NEUROSCIENCE, 1994, 60 (01) :263-273

[4] Differential blood-brain barrier breakdown and leucocyte recruitment following excitotoxic lesions in juvenile and adult rats [J].

Bolton, SJ ;

Perry, VH .

EXPERIMENTAL NEUROLOGY, 1998, 154 (01) :231-240

[5] Spatiotemporal patterns of postsynaptic density (PSD)-95 expression after rat spinal cord injury [J].

Cheng, C. ;

Gao, S. ;

Zhao, J. ;

Niu, S. ;

Chen, M. ;

Li, X. ;

Qin, J. ;

Shi, S. ;

Guo, Z. ;

Shen, A. .

NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY, 2008, 34 (03) :340-356

[6] Axon pathology in neurological disease: a neglected therapeutic target [J].

Coleman, MP ;

Perry, VH .

TRENDS IN NEUROSCIENCES, 2002, 25 (10) :532-537

[7] Changes of cytoskeletal protein immunostaining in myelinated fibre tracts after focal cerebral ischaemia in the rat [J].

Dewar, D ;

Dawson, DA .

ACTA NEUROPATHOLOGICA, 1997, 93 (01) :71-77

[8] Drug development for stroke: importance of protecting cerebral white matter [J].

Dewar, D ;

Yam, P ;

McCulloch, J .

EUROPEAN JOURNAL OF PHARMACOLOGY, 1999, 375 (1-3) :41-50

[9] Differential patterns of inflammatory response, axonal damage and myelin impairment following excitotoxic or ischemic damage to the trigeminal spinal nucleus of adult rats [J].

Dos Santos, C. D. ;

Picanco-Diniz, C. W. ;

Gomes-Leal, W. .

BRAIN RESEARCH, 2007, 1172 :130-144

[10] Apoptosis after traumatic human spinal cord injury [J].

Emery, E ;

Aldana, P ;

Bunge, MB ;

Puckett, W ;

Srinivasan, A ;

Keane, RW ;

Bethea, J ;

Levi, ADO .

JOURNAL OF NEUROSURGERY, 1998, 89 (06) :911-920

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