TNF-α contributes to axonal sprouting and functional recovery following traumatic brain injury

被引:56
作者
Oshima, Taku [2 ,3 ]
Lee, Sachiko [1 ]
Sato, Akinobu [1 ]
Oda, Shigeto [3 ]
Hirasawa, Hiroyuki [3 ]
Yamashita, Toshihide [1 ,2 ]
机构
[1] Osaka Univ, Grad Sch Med, Dept Mol Neurosci, Suita, Osaka 5650871, Japan
[2] Chiba Univ, Grad Sch Med, Dept Neurobiol, Chiba, Japan
[3] Chiba Univ, Grad Sch Med, Dept Emergency & Crit Care Med, Chiba, Japan
关键词
Axon; Brain injury; Motor function; Regeneration; TNF-alpha; TUMOR-NECROSIS-FACTOR; CLOSED-HEAD INJURY; RAT-BRAIN; MICE LACKING; EXPRESSION; RECEPTOR; PLASTICITY; ELEVATION; RESPONSES; PLASMA;
D O I
10.1016/j.brainres.2009.07.022
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
In response to a central nervous system (CNS) injury, microglia and astrocytes release tumor necrosis factor-alpha (TNF-alpha). This proinflammatory cytokine has been implicated in both neuronal cell death and survival. Here, we show that TNF-alpha is involved in the recovery of neuromotor function following traumatic brain injury. Composite neuroscore and accel rotarod were employed to measure neuromotor function. TNF-alpha-deficient (TNF-alpha(-/-)) mice showed no improvement in their locomotor function up to 28 days following controlled cortical impact brain injury. Although collateral sprouting of the unlesioned corticospinal tract, as assessed by retrograde biotin dextran amine labeling, at the cervical spinal cord was observed following injury in the wild-type mice, such changes were not induced in the TNF-alpha(-/-) mice at 4 weeks after injury. These results provide evidence that TNF-alpha is involved in neuroanatomical plasticity and functional recovery following CNS injury. (C) 2009 Elsevier B.V. All rights reserved.
引用
收藏
页码:102 / 110
页数:9
相关论文
共 24 条
[1]  
BERMPOHL D, 2007, J CEREB BLOOD FLOW M, V27, P1669
[2]   Miracles and molecules - progress in spinal cord repair [J].
Blight, AR .
NATURE NEUROSCIENCE, 2002, 5 (Suppl 11) :1051-1054
[3]   Altered neuronal and microglial responses to excitotoxic and ischemic brain injury in mice lacking TNF receptors [J].
Bruce, AJ ;
Boling, W ;
Kindy, MS ;
Peschon, J ;
Kraemer, PJ ;
Carpenter, MK ;
Holtsberg, FW ;
Mattson, MP .
NATURE MEDICINE, 1996, 2 (07) :788-794
[4]   Extensive cortical rewiring after brain injury [J].
Dancause, N ;
Barbay, S ;
Frost, SB ;
Plautz, EJ ;
Chen, DF ;
Zoubina, EV ;
Stowe, AM ;
Nudo, RJ .
JOURNAL OF NEUROSCIENCE, 2005, 25 (44) :10167-10179
[5]   Experimental brain injury induces differential expression of tumor necrosis factor-alpha mRNA in the CNS [J].
Fan, L ;
Young, PR ;
Barone, FC ;
Feuerstein, GZ ;
Smith, DH ;
McIntosh, TK .
MOLECULAR BRAIN RESEARCH, 1996, 36 (02) :287-291
[6]   Ischemic and excitotoxic brain injury is enhanced in mice lacking the p55 tumor necrosis factor receptor [J].
Gary, DS ;
Bruce-Keller, AJ ;
Kindy, MS ;
Mattson, MP .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1998, 18 (12) :1283-1287
[7]  
GOODMAN JC, 1990, J NEUROIMMUNOL, V30, P213
[8]   Delayed cytokine expression in rat brain following experimental contusion [J].
Holmin, S ;
Schalling, M ;
Hojeberg, B ;
Nordqvist, ACS ;
Skeftruna, AK ;
Mathiesen, T .
JOURNAL OF NEUROSURGERY, 1997, 86 (03) :493-504
[9]   The expression of tumor necrosis factor-alpha in the rat brain after fluid percussive injury [J].
Kita, T ;
Liu, L ;
Tanaka, N ;
Kinoshita, Y .
INTERNATIONAL JOURNAL OF LEGAL MEDICINE, 1997, 110 (06) :305-311
[10]   Nogo receptor antagonism promotes stroke recovery by enhancing axonal plasticity [J].
Lee, JK ;
Kim, JE ;
Sivula, M ;
Strittmatter, SM .
JOURNAL OF NEUROSCIENCE, 2004, 24 (27) :6209-6217