Delayed Glial Cell Death Following Wallerian Degeneration in White Matter Tracts after Spinal Cord Dorsal Column Cordotomy in Adult Rats

Warden, Patricia; Bamber, Norman I.; Li, Huaying; Esposito, Andrew C.; Ahmad, Kaashif A.; Hsu, Chung Y.; Xu, Xiao–Ming

doi:10.1006/exnr.2000.7622

Cited by 123 publications

(96 citation statements)

References 31 publications

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“…1C4,C5). Some large myelinated axons were observed in the dCST caudal to the lesion site as reported previously (Warden et al, 2001). These axons were generally larger than in intact animals; the mean cross-sectional area of these residual axons was 0.58 Ϯ 0.03 m 2 (n ϭ 11) compared with 0.29 Ϯ 0.01 m 2 (n ϭ 4) for the intact dCST.…”

Section: Histology Of Dorsal Funiculus In Control and Transected Spinsupporting

confidence: 82%

Identified Olfactory Ensheathing Cells Transplanted into the Transected Dorsal Funiculus Bridge the Lesion and Form Myelin

Sasaki

Lankford²,

Zemedkun³

et al. 2004

J. Neurosci.

143

118

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Olfactory ensheathing cells (OECs) prepared from the olfactory bulbs of adult transgenic Sprague Dawley (SD) rats expressing green fluorescent protein (GFP) were transplanted into a dorsal spinal cord transection lesion of SD rats. Five weeks after transplantation, the cells survived within the lesion zone and oriented longitudinally along axons that bridged the transection site. Although the highest density of GFP cells was within the lesion zone, some cells distributed longitudinally outside of the lesion area. Myelinated axons spanning the lesion were observed in discrete bundles encapsulated by a cellular element. Electron micrographs of spinal cords immunostained with an anti-GFP antibody indicated that a majority of the peripheral-like myelinated axons were derived from donor OECs. Open-field locomotor behavior was significantly improved in the OEC transplantation group. Thus, transplanted OECs derived from the adult olfactory bulb can survive and orient longitudinally across a spinal cord transection site and form myelin. This pattern of repair is associated with improved locomotion.

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Section: Histology Of Dorsal Funiculus In Control and Transected Spinsupporting

confidence: 82%

Identified Olfactory Ensheathing Cells Transplanted into the Transected Dorsal Funiculus Bridge the Lesion and Form Myelin

Sasaki

Lankford²,

Zemedkun³

et al. 2004

J. Neurosci.

143

118

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“…The concurrent loss of oligodendrocytes in degenerating axon tracts suggests an intimate relationship between oligodendrocyte survival and axonal integrity (Barres et al, 1993;Crowe et al, 1997;Warden et al, 2001). Since oligodendrocytes myelinate several axons simultaneously, the loss of a single cell can influence neighboring axons.…”

Section: Discussionmentioning

confidence: 99%

Neuropsin promotes oligodendrocyte death, demyelination and axonal degeneration after spinal cord injury

et al. 2007

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Abbreviations: SCI, spinal cord injury; DIG, digoxigenin; APC, adenomatus polyposis coli; MBP, myelin basic protein; TUNEL, TdT-mediated dUTP-fluorescein nick end labeling -3 - AbstractPrevious studies indicated that the expression of neuropsin, a serine protease, is induced in mature oligodendrocytes after injury to the central nervous system (CNS). The pathophysiology of spinal cord injury (SCI) involves primary and secondary mechanisms, the latter contributing further to permanent losses of function. To explore the role of neuropsin after SCI, histochemical and behavioral analyses were performed in wild-type (WT) and neuropsin-deficient (neuropsin -/-) mice using a crush injury model, a well-characterized and consistently reproducible model of SCI. In situ hybridization revealed that neuropsin mRNA expression was induced in the spinal cord white matter from WT mice after crush SCI, peaking at day 4. Neuropsin -/-mice showed attenuated demyelination, oligodendrocyte death, and axonal damage after SCI.Although axonal degeneration in the corticospinal tract was obvious caudal to the lesion site in both strains of mice after SCI, the number of surviving nerve fibers caudal to the lesion was significantly larger in neuropsin -/-mice than WT mice. Behavioral analysis revealed that the recovery at days 10-42 was significantly improved in neuropsin -/-mice compared to WT mice in spite of the severe initial hindlimb impairments due to SCI in both strains. These observations suggest that neuropsin is involved in the secondary phase of the pathogenesis of SCI mediated by demyelination, oligodendrocyte death, and axonal degeneration.-4 -

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“…33,34 Oligodendroglial apoptosis is known to be associated with upregulation of caspase-3 for signaling in apoptosis 35 as well as FAS and p75 expression, 36 and has been shown to be related to progression of white matter degeneration. 37 In other words, the decrease of apoptotic cell death by hypothermia may reduce myelin damage, and contribute to the recovery of neurologic function. Previous studies reported that administration of MK-801 and/or a competitive inhibitor (l-Ng-nitro-arginine methylester) of nitric oxide synthase (NOS) resulted in a reduction of TPC following SCI.…”

Section: Discussionmentioning

confidence: 99%

Post-traumatic moderate systemic hypothermia reduces TUNEL positive cells following spinal cord injury in rat

et al. 2004

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Study design: A standardized animal model of contusive spinal cord injury (SCI) with incomplete paraplegia was used to test the hypothesis that moderate systemic hypothermia reduces neural cell death. Terminal deoxynucleotidyl transferase [TdT]-mediated deoxyuridine triphosphate [dUTP] nick-end labeling (TUNEL) staining was used as a marker of apoptosis or cell damage. Objective: To determine whether or not moderate hypothermia could have a neuroprotective effect in neural cell death following spinal cord injury in rats. Setting: Kagawa Medical University, Japan. Methods: Male Sprague-Dawley (SD) rats (n ¼ 39) weighing on average 300 g (280-320 g) were used to prepare SCI models. After receiving contusive injury at T11/12, rats were killed at 24 h, 72 h, or 7 days after injury. The spinal cord was removed en bloc and of examined at five segments: 5 and 10 mm rostral to the center of injury, center of injury, and 5 and 10 mm caudal to the center of injury. Rats that received hypothermia (321C/4 h) were killed at the same time points as those that received normothermia (371C/3 h). The specimens were stained with hematoxylin and eosin, and subjected to in situ nick-end labeling (TUNEL), a specific method for visualizing cell death in the spinal cord. Results: At 24 h postinjury, TUNEL positive cells (TPC) decreased significantly 10 mm rostral to center of injury in hypothermic animals compared to the normothermia group. At 72 h post-SCI, TPC also decreased significantly at 5 mm rostral, and 5 and 10 mm caudal to the lesion center compared to normothermic animals. At 7 days postinjury, a significant decrease of TPC was observed at the 5 mm rostral and 5 mm caudal sites compared to normothermic animals. Conclusion: These results indicate that systemic hypothermia has a neuroprotective effect following SCI by attenuating post-traumatic TPC.

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Delayed Glial Cell Death Following Wallerian Degeneration in White Matter Tracts after Spinal Cord Dorsal Column Cordotomy in Adult Rats

Cited by 123 publications

References 31 publications

Identified Olfactory Ensheathing Cells Transplanted into the Transected Dorsal Funiculus Bridge the Lesion and Form Myelin

Identified Olfactory Ensheathing Cells Transplanted into the Transected Dorsal Funiculus Bridge the Lesion and Form Myelin

Neuropsin promotes oligodendrocyte death, demyelination and axonal degeneration after spinal cord injury

Post-traumatic moderate systemic hypothermia reduces TUNEL positive cells following spinal cord injury in rat

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