Reactions of oligodendrocytes to spinal cord injury: Cell survival and myelin repair

被引:50
作者
Frei, E
Klusman, I
Schnell, L
Schwab, ME
机构
[1] Univ Zurich, Brain Res Inst, Dept Neuromorphol, CH-8057 Zurich, Switzerland
[2] Swiss Fed Inst Technol, CH-8057 Zurich, Switzerland
关键词
oligodendrocytes; inflammation; macrophages; proteolipid protein; spinal cord injury; rat;
D O I
10.1006/exnr.2000.7379
中图分类号
Q189 [神经科学];
学科分类号
071006 [神经生物学];
摘要
The aim of this study was to elucidate whether oligodendrocytes die in fiber tracts that are spared by a spinal cord injury but are in close vicinity of inflammatory cells. Adult rat spinal cords were studied histologically 1 day to 2 weeks after a contusion lesion that left the ventral white matter largely intact. Massive oligodendrocyte death occurred in the lesion center, along with the death of neurons, microglia, and astrocytes. Oligodendrocytes, specifically positive for proteolipid protein (PLP) mRNA, were counted in the ventral white matter where axons at the rostral and caudal edges of the lesion were histologically intact. Although these regions contained many macrophages and neutrophils hypothesized to contribute to secondary tissue loss, there was no significant loss of oligodendrocytes. In the ventral funiculus, 3 and 6 mm rostral and caudal to the lesion, oligodendrocyte numbers were also unchanged, in spite of the presence of many activated microglial cells. From day 7 on, oligodendrocytes in close vicinity to the lesion increased their expression of PLP mRNA. We conclude that, at least within the first 2 weeks after a spinal cord contusion lesion, there is no major devastating influence of inflammatory cells or their mediators on oligodendrocytes. When death occurs, it may be due to mechanical trauma, ischemia, or excitotoxicity within the lesion or it may occur as a result of axonal degeneration. (C) 2000 Academic Press.
引用
收藏
页码:373 / 380
页数:8
相关论文
共 41 条
[1]
Amat JA, 1998, GLIA, V22, P64, DOI 10.1002/(SICI)1098-1136(199801)22:1<64::AID-GLIA6>3.0.CO
[2]
2-8
[3]
Ciliary neurotrophic factor enhances the rate of oligodendrocyte generation [J].
Barres, BA ;
Burne, JF ;
Holtmann, B ;
Thoenen, H ;
Sendtner, M ;
Raff, MC .
MOLECULAR AND CELLULAR NEUROSCIENCE, 1996, 8 (2-3) :146-156
[4]
Bartholdi D, 1998, GLIA, V23, P278, DOI 10.1002/(SICI)1098-1136(199807)23:3<278::AID-GLIA10>3.0.CO
[5]
2-Q
[6]
Expression of pro-inflammatory cytokine and chemokine mRNA upon experimental spinal cord injury in mouse: An in situ hybridization study [J].
Bartholdi, D ;
Schwab, ME .
EUROPEAN JOURNAL OF NEUROSCIENCE, 1997, 9 (07) :1422-1438
[7]
Graded histological and locomotor outcomes after spinal cord contusion using the NYU weight-drop device versus transection [J].
Basso, DM ;
Beattie, MS ;
Bresnahan, JC .
EXPERIMENTAL NEUROLOGY, 1996, 139 (02) :244-256
[8]
MODELING OF ACUTE SPINAL-CORD INJURY IN THE RAT - NEUROPROTECTION AND ENHANCED RECOVERY WITH METHYLPREDNISOLONE, U-74006F AND YM-14673 [J].
BEHRMANN, DL ;
BRESNAHAN, JC ;
BEATTIE, MS .
EXPERIMENTAL NEUROLOGY, 1994, 126 (01) :61-75
[9]
Bhat RV, 1996, GLIA, V17, P169
[10]
Animal models of demyelination [J].
Bradl, M ;
Linington, C .
BRAIN PATHOLOGY, 1996, 6 (03) :303-311