Autonomic dysreflexia after spinal cord transection or compression in 129Sv, C57BL, and Wallerian degeneration slow mutant mice

Jacob, Jasmine; Gris, Paul; Fehlings, Michael G.; Weaver, Lynne C.; Brown, Arthur

doi:10.1016/s0014-4886(03)00161-4

Cited by 27 publications

(16 citation statements)

References 36 publications

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“…This result is in line with a previous observation showing the occurrence of local sprouting of primary afferent nociceptive fibers caudal to a spinal cord lesion in Sv129 but not in BL/6 mice (Jacob et al, 2003). The present data therefore clearly show a major regeneration-enhancing effect of Nogo-A deletion in mice and a strong influence of the genetic background.…”

Section: Discussionsupporting

confidence: 94%

Nogo-A-Deficient Mice Reveal Strain-Dependent Differences in Axonal Regeneration

Dimou¹,

Schnell²,

Montani³

et al. 2006

J. Neurosci.

151

130

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Nogo-A, a membrane protein enriched in myelin of the adult CNS, inhibits neurite growth and regeneration; neutralizing antibodies or receptor blockers enhance regeneration and plasticity in the injured adult CNS and lead to improved functional outcome. Here we show that Nogo-A-specific knock-outs in backcrossed 129X1/SvJ and C57BL/6 mice display enhanced regeneration of the corticospinal tract after injury. Surprisingly, 129X1/SvJ Nogo-A knock-out mice had two to four times more regenerating fibers than C57BL/6 Nogo-A knock-out mice. Wild-type newborn 129X1/SvJ dorsal root ganglia in vitro grew a much higher number of processes in 3 d than C57BL/6 ganglia, confirming the stronger endogenous neurite growth potential of the 129X1/SvJ strain. cDNA microarrays of the intact and lesioned spinal cord of wild-type as well as Nogo-A knock-out animals showed a number of genes to be differentially expressed in the two mouse strains; many of them belong to functional categories associated with neurite growth, synapse formation, and inflammation/ immune responses. These results show that neurite regeneration in vivo, under the permissive condition of Nogo-A deletion, and neurite outgrowth in vitro differ significantly in two widely used mouse strains and that Nogo-A is an important endogenous inhibitor of axonal regeneration in the adult spinal cord.

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Section: Discussionsupporting

confidence: 94%

Nogo-A-Deficient Mice Reveal Strain-Dependent Differences in Axonal Regeneration

Dimou¹,

Schnell²,

Montani³

et al. 2006

J. Neurosci.

151

130

View full text Add to dashboard Cite

show abstract

“…After 10 min, the mice were anesthetized by induction with 4% halothane and maintained with 1.5% halothane. The T4 spinal cord segment was exposed by dorsal laminectomy and injured, without disrupting the dura, by a 60-sec 8.3-g clip compression (Jacob et al, 2003;Joshi and Fehlings, 2002). The skin was closed and the injured mice were allowed to recover under a heat lamp.…”

Section: Spinal Cord Injurymentioning

confidence: 99%

CD11d Antibody Treatment Improves Recovery in Spinal Cord-Injured Mice

Geremia

Feng²,

Rosenzweig³

et al. 2012

Journal of Neurotrauma

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Acute administration of a monoclonal antibody (mAb) raised against the CD11d subunit of the leukocyte CD11d/CD18 integrin after spinal cord injury (SCI) in the rat greatly improves neurological outcomes. This has been chiefly attributed to the reduced infiltration of neutrophils into the injured spinal cord in treated rats. More recently, treating spinal cord-injured mice with a Ly-6G neutrophil-depleting antibody was demonstrated to impair neurological recovery. These disparate results could be due to different mechanisms of action utilized by the two antibodies, or due to differences in the inflammatory responses between mouse and rat that are triggered by SCI. To address whether the anti-CD11d treatment would be effective in mice, a CD11d mAb (205C) or a control mAb (1B7) was administered intravenously at 2, 24, and 48 h after an 8-g clip compression injury at the fourth thoracic spinal segment. The anti-CD11d treatment reduced neutrophil infiltration into the injured mouse spinal cord and was associated with increased white matter sparing and reductions in myeloperoxidase (MPO) activity, reactive oxygen species, lipid peroxidation, and scar formation. These improvements in the injured spinal cord microenvironment were accompanied by increased serotonin (5-HT) immunoreactivity below the level of the lesion and improved locomotor recovery. Our results with the 205C CD11d mAb treatment complement previous work using this anti-integrin treatment in a rat model of SCI.

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“…It has recently been demonstrated in animals that the development and severity of AD can be significantly attenuated by administering neuroprotective strategies acutely after spinal injury. 32,33 Additionally, it is known that sprouting of primary afferent fibers after SCI is part of the mechanism underlying the development of AD in rodents [34][35][36][37][38] and that administering anti-nerve growth factor (NGF) intraspinally can block AD. 39 Very recently, it was further demonstrated that adenoviraloverexpression of NGF (growth-promoting) or semaphorin 3A (Sema3a, growth-inhibiting), intraspinally, increased or decreased the postinjury sprouting of primary afferent fibers caudal to the lesion, respectively.…”

Section: Improving Sexual Function Is Important Irrespective Of Multmentioning

confidence: 99%

The impact of spinal cord injury on sexual function: concerns of the general population

et al. 2006

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Study Design: Secure, web-based survey. Objectives: Obtain information from the spinal cord injured (SCI) population regarding sexual dysfunctions, with the aim of developing new basic science and clinical research and eventual therapies targeting these issues. Setting: Worldwide web. Methods: Individuals 18 years or older living with SCI. Participants obtained a pass-code to enter a secure website and answered survey questions. A total of 286 subjects completed the survey. Results: The majority of participants stated that their SCI altered their sexual sense of self and that improving their sexual function would improve their quality of life (QoL). The primary reason for pursuing sexual activity was for intimacy need, not fertility. Bladder and bowel concerns during sexual activity were not strong enough to deter the majority of the population from engaging in sexual activity. However, in the subset of individuals concerned about bladder and/or bowel incontinence during sexual activity, this was a highly significant issue. In addition, the occurrence of autonomic dysreflexia (AD) during typical bladder or bowel care was a significant variable predicting the occurrence and distress of AD during sexual activity. Conclusion: Sexual function and its resultant impact on QoL is a major issue to an overwhelming majority of people living with SCI. This certainly constitutes the need for expanding research in multiple aspects to develop future therapeutic interventions for sexual health and SCI.

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Autonomic dysreflexia after spinal cord transection or compression in 129Sv, C57BL, and Wallerian degeneration slow mutant mice

Cited by 27 publications

References 36 publications

Nogo-A-Deficient Mice Reveal Strain-Dependent Differences in Axonal Regeneration

Nogo-A-Deficient Mice Reveal Strain-Dependent Differences in Axonal Regeneration

CD11d Antibody Treatment Improves Recovery in Spinal Cord-Injured Mice

The impact of spinal cord injury on sexual function: concerns of the general population

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