Autonomic and motor neuron death is progressive and parallel in a lumbosacral ventral root avulsion model of cauda equina injury

2003 ◽  
Vol 467 (4) ◽  
pp. 477-486 ◽  
Author(s):  
Thao X. Hoang ◽  
Jaime H. Nieto ◽  
Niranjala J.K. Tillakaratne ◽  
Leif A. Havton
Keyword(s):  
Motor Neuron ◽  
Cauda Equina ◽  
Ventral Root ◽  
Root Avulsion ◽  
Neuron Death ◽  
Ventral Root Avulsion ◽  
Motor Neuron Death

scholarly journals Modulation of the visceromotor reflex by a lumbosacral ventral root avulsion injury and repair in rats

2012 ◽  
Vol 303 (5) ◽  
pp. F641-F647 ◽  
Author(s):  
Huiyi H. Chang ◽  
Leif A. Havton
Keyword(s):  
Cauda Equina ◽  
Experimental Models ◽  
Ventral Root ◽  
Oblique Muscle ◽  
Emg Activity ◽  
Noxious Stimulation ◽  
Electromyographic Activity ◽  
Root Avulsion ◽  
Contraction Duration ◽  
Ventral Root Avulsion

Increased abdominal muscle wall activity may be part of a visceromotor reflex (VMR) response to noxious stimulation of the bladder. However, information is sparse regarding the effects of cauda equina injuries on the VMR in experimental models. We studied the effects of a unilateral L6-S1 ventral root avulsion (VRA) injury and acute ventral root reimplantation (VRI) into the spinal cord on micturition reflexes and electromyographic activity of the abdominal wall in rats. Cystometrogram (CMG) and electromyography (EMG) of the abdominal external oblique muscle (EOM) were performed. All rats demonstrated EMG activity of the EOM associated with reflex bladder contractions. At 1 wk after VRA and VRI, the duration of the EOM EMG activity associated with reflex voiding was significantly prolonged compared with age-matched sham rats. However, at 3 wk postoperatively, the duration of the EOM responses remained increased in the VRA series but had normalized in the VRI group. The EOM EMG duration was normalized for both VRA and VRI groups at 8–12 wk postoperatively. CMG recordings show increased contraction duration at 1 and 3 wk postoperatively for the VRA series, whereas the contraction duration was only increased at 1 wk postoperatively for the VRI series. Our studies suggest that a unilateral lumbosacral VRA injury results in a prolonged VMR to bladder filling using a physiological saline solution. An acute root replantation decreased the VMR induced by VRA injury and provides earlier sensory recovery.

scholarly journals Oligodendrocytes contribute to motor neuron death in ALS via SOD1-dependent mechanism

2016 ◽  
Vol 113 (42) ◽  
pp. E6496-E6505 ◽  
Author(s):  
Laura Ferraiuolo ◽  
Kathrin Meyer ◽  
Thomas W. Sherwood ◽  
Jonathan Vick ◽  
Shibi Likhite ◽  
...  
Keyword(s):  
Motor Neuron ◽  
Lactate Production ◽  
Chromosome 9 ◽  
Neuron Death ◽  
Motor Neuron Death ◽  
Repeat Expansions ◽  
Human Oligodendrocytes ◽  
Lateral Sclerosis ◽  
Dependent Mechanism

Oligodendrocytes have recently been implicated in the pathophysiology of amyotrophic lateral sclerosis (ALS). Here we show that, in vitro, mutant superoxide dismutase 1 (SOD1) mouse oligodendrocytes induce WT motor neuron (MN) hyperexcitability and death. Moreover, we efficiently derived human oligodendrocytes from a large number of controls and patients with sporadic and familial ALS, using two different reprogramming methods. All ALS oligodendrocyte lines induced MN death through conditioned medium (CM) and in coculture. CM-mediated MN death was associated with decreased lactate production and release, whereas toxicity in coculture was lactate-independent, demonstrating that MN survival is mediated not only by soluble factors. Remarkably, human SOD1 shRNA treatment resulted in MN rescue in both mouse and human cultures when knockdown was achieved in progenitor cells, whereas it was ineffective in differentiated oligodendrocytes. In fact, early SOD1 knockdown rescued lactate impairment and cell toxicity in all lines tested, with the exclusion of samples carrying chromosome 9 ORF 72 (C9orf72) repeat expansions. These did not respond to SOD1 knockdown nor did they show lactate release impairment. Our data indicate that SOD1 is directly or indirectly involved in ALS oligodendrocyte pathology and suggest that in this cell type, some damage might be irreversible. In addition, we demonstrate that patients with C9ORF72 represent an independent patient group that might not respond to the same treatment.

scholarly journals Combining timed GDNF and ChABC gene therapy to promote long‐distance regeneration following ventral root avulsion and repair

2020 ◽  
Vol 34 (8) ◽  
pp. 10605-10622 ◽  
Author(s):  
Ruben Eggers ◽  
Fred Winter ◽  
Lotte Smit ◽  
Maruelle Luimens ◽  
Elizabeth M. Muir ◽  
...  
Keyword(s):  
Gene Therapy ◽  
Ventral Root ◽  
Root Avulsion ◽  
Long Distance ◽  
Ventral Root Avulsion

scholarly journals Neuroprotection and Axonal Regeneration After Lumbar Ventral Root Avulsion by Re-implantation and Mesenchymal Stem Cells Transplant Combined Therapy

2013 ◽  
Vol 10 (2) ◽  
pp. 354-368 ◽  
Author(s):  
Abel Torres-Espín ◽  
Dora Luz Corona-Quintanilla ◽  
Joaquim Forés ◽  
Ilary Allodi ◽  
Francisco González ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Axonal Regeneration ◽  
Combined Therapy ◽  
Ventral Root ◽  
Root Avulsion ◽  
Ventral Root Avulsion

Delayed selective motor neuron death and Fas antigen induction after spinal cord ischemia in rabbits

1998 ◽  
Vol 797 (1) ◽  
pp. 23-28 ◽  
Author(s):  
Masahiro Sakurai ◽  
Takeshi Hayashi ◽  
Koji Abe ◽  
Mitsuaki Sadahiro ◽  
Koichi Tabayashi
Keyword(s):  
Spinal Cord ◽  
Motor Neuron ◽  
Spinal Cord Ischemia ◽  
Neuron Death ◽  
Fas Antigen ◽  
Motor Neuron Death
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