Unilateral induction of progenitors in the spinal cord of hSOD1G93A transgenic rats correlates with an asymmetrical hind limb paralysis

2006 ◽  
Vol 401 (1-2) ◽  
pp. 25-29 ◽  
Author(s):  
Isabelle de Hemptinne ◽  
Cédric Boucherie ◽  
Roland Pochet ◽  
Kadiombo Bantubungi ◽  
Serge N. Schiffmann ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Hind Limb ◽  
Transgenic Rats ◽  
Hind Limb Paralysis

Canine spinal nephroblastoma

1997 ◽  
Vol 33 (4) ◽  
pp. 302-306 ◽  
Author(s):  
NP Macri ◽  
W Van Alstine ◽  
RA Coolman
Keyword(s):  
Spinal Cord ◽  
Hind Limb ◽  
Spinal Column ◽  
Plain Radiographs ◽  
Clinically Normal ◽  
Mixed Breed ◽  
Hind Limb Paralysis

An eight-month-old, female, mixed-breed dog was presented with bilateral hind-limb paralysis that reportedly developed over a two-to-three week period and was not associated with trauma. Plain radiographs of the spinal column were unremarkable, and a myelogram outlined an intramedullary mass of the spinal cord at the first lumbar (L1) vertebra. A hemilaminectomy was performed, and a mass that was identified histologically as nephroblastoma was excised from the spinal cord. Following surgery, the dog became fully ambulatory, and at 22 months postsurgery she remains clinically normal. The diagnosis, treatment, progression, histogenesis, and pathology of canine nephroblastoma are discussed.

scholarly journals RIP2-mediated LKB1 deletion causes axon degeneration in the spinal cord and hind-limb paralysis

2010 ◽  
Vol 4 (2) ◽  
pp. 193-202 ◽  
Author(s):  
G. Sun ◽  
R. Reynolds ◽  
I. Leclerc ◽  
G. A. Rutter
Keyword(s):  
Spinal Cord ◽  
Hind Limb ◽  
Axon Degeneration ◽  
Hind Limb Paralysis

scholarly journals BCL-2 and BAX Protect Adult Mice from Lethal Sindbis Virus Infection but Do Not Protect Spinal Cord Motor Neurons or Prevent Paralysis

2002 ◽  
Vol 76 (20) ◽  
pp. 10393-10400 ◽  
Author(s):  
Douglas A. Kerr ◽  
Thomas Larsen ◽  
Susan H. Cook ◽  
Yih-Ru Fannjiang ◽  
Eunkyung Choi ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Cell Death ◽  
Motor Neurons ◽  
Hind Limb ◽  
Sindbis Virus ◽  
Apoptotic Cell ◽  
Lumbar Spinal Cord ◽  
Newborn Mice ◽  
Adult Mice ◽  
Hind Limb Paralysis

ABSTRACT Cellular proteins that regulate apoptotic cell death can modulate the outcome of Sindbis virus (SV) encephalitis in mice. Both endogenous and overexpressed BCL-2 and BAX proteins protect newborn mice from fatal SV infection by blocking apoptosis in infected neurons. To determine the effects of these cellular factors on the course of infection in older animals, a more neurovirulent SV vector (dsNSV) was constructed from a viral strain that causes both prominent spinal cord infection with hind-limb paralysis and death in weanling mice. This vector has allowed assessment of the effects of BCL-2 and BAX on both mortality and paralysis in these hosts. Similar to newborn hosts, weanling mice infected with dsNSV encoding BCL-2 or BAX survived better than animals infected with control viruses. This finding indicates that BCL-2 and BAX both protect neurons that mediate host survival. Neither cellular factor, however, could suppress the development of hind-limb paralysis or prevent the degeneration of motor neurons in the lumbar spinal cord. Infection of BAX knockout mice with dsNSV demonstrated that endogenous BAX also enhances the survival of animals but has no effect on paralysis. These findings for the spinal cord are consistent with earlier data showing that dying lumbar motor neurons do not exhibit an apoptotic morphology. Thus, divergent cell death pathways are activated in different target populations of neurons during neurovirulent SV infection of weanling mice.

scholarly journals The Role of IL-17 Promotes Spinal Cord Neuroinflammation via Activation of the Transcription Factor STAT3 after Spinal Cord Injury in the Rat

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Shaohui Zong ◽  
Gaofeng Zeng ◽  
Ye Fang ◽  
Jinzhen Peng ◽  
Yong Tao ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Hind Limb ◽  
Rating Scale ◽  
Serum Levels ◽  
Spinal Cord Tissue ◽  
Expression Levels ◽  
Stat3 Signaling ◽  
Cord Injury ◽  
Disease Stages

Study Design.In this study, we investigated the role of IL-17 via activation of STAT3 in the pathophysiology of SCI.Objective.The purpose of the experiments is to study the expression of IL-17 and related cytokines via STAT3 signaling pathways, which is caused by the acute inflammatory response following SCI in different periods via establishing an acute SCI model in rat.Methods.Basso, Beattie, and Bresnahan hind limb locomotor rating scale was used to assess the rat hind limb motor function. Immunohistochemistry was used to determine the expression levels of IL-17 and p-STAT3 in spinal cord tissues. Western blotting analysis was used to determine the protein expression of p-STAT3 in spinal cord tissue. RT-PCR was used to analyze the mRNA expression of IL-17 and IL-23p19 in the spleen tissue. ELISA was used to determine the peripheral blood serum levels of IL-6, IL-21, and IL-23.Results.Compared to the sham-operated group, the expression levels of IL-17, p-STAT3, IL-6, IL-21, and IL-23 were significantly increased and peaked at 24 h after SCI. The increased levels of cytokines were correlated with the SCI disease stages.Conclusion.IL-17 may play an important role in promoting spinal cord neuroinflammation after SCI via activation of STAT3.

Motor projection patterns to the hind limb of normal and paralysed chick embryos

Development ◽  
1982 ◽  
Vol 72 (1) ◽  
pp. 269-286
Author(s):  
N. G. Laing
Keyword(s):  
Spinal Cord ◽  
Cell Death ◽  
Hind Limb ◽  
Muscle Volume ◽  
Chick Embryos ◽  
Relative Contribution ◽  
Hind Limbs ◽  
Lateral Motor Column ◽  
Before And After ◽  
Major Period

Counts were made of the number of motoneurons innervating the hind limbs of 10-day normal and paralysed chick embryos whose right hind limb buds had been subjected to varying degrees of amputation prior to innervation. The number of motoneurons on the intact sides of the paralysed embryos was found to be similar to the number present in normal embryos prior to the major period of motoneuron death. Since it has previously been shown that paralysis does not increase the number of motoneurons generated, this means that normal motoneuron death was largely prevented in the paralysed embryos. There were differences in the distributions of motoneurons in the rostrocaudal axis of the spinal cord between normal and paralysed embryos. Therefore, cell death does not eliminate a uniform fraction of motoneurons throughout the rostrocaudal extent of the chick embryo lumbar lateral motor column. It is also argued that there are differences in the relative contribution of the various lumbosacral levels to different parts of the limb, e.g. the shank, before and after the period of cell death. In both normal and paralysed embryos there was a linear relationship between the volume of limb muscle which developed after amputation and the number of motoneurons surviving in the spinal cord. There was no evidence of a ‘compression’ of motoneurons into the remaining muscle either after amputation alone or after amputation combined with paralysis. Motoneurons are therefore rigidly specified for certain parts of the limb. The relationship between motoneuron number and muscle volume on the amputated side differed from that of the intact side. For a similar increase in muscle volume there was a smaller increase in motoneuron number on the intact sides. This suggested a parallel to the paradoxically small increase in motoneuron number that occurs on the addition of a supernumerary limb.

scholarly journals Slow- and fast-twitch rat hind limb skeletal muscle phenotypes 8 months after spinal cord transection and olfactory ensheathing glia transplantation

2008 ◽  
Vol 586 (10) ◽  
pp. 2593-2610 ◽  
Author(s):  
Pilar Negredo ◽  
José-Luis L. Rivero ◽  
Beatriz González ◽  
Almudena Ramón-Cueto ◽  
Rafael Manso
Keyword(s):  
Skeletal Muscle ◽  
Spinal Cord ◽  
Hind Limb ◽  
Spinal Cord Transection ◽  
Olfactory Ensheathing Glia ◽  
Fast Twitch
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