ArticleVentral horn motoneurons 10, 20 and 52 weeks after T-9 spinal cord transection
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Phrenic motor neuron survival below cervical spinal cord hemisection
2021, Experimental NeurologyCitation Excerpt :While some of the disparities observed across studies are likely related to differences in injury type and/or severity, the methods used to evaluate motor neuron survival may also contribute. Indeed, methods used to assess neuronal survival post-injury vary considerably across studies, ranging from retrograde tracing methods (fluoro‑gold, horseradish peroxidase, CtB) to immunohistochemistry/staining methods such as hematoxaline and eosin, Cresyl violet, TUNEL, ChAT, etc. (Bose et al., 2005; Eidelberg et al., 1989; Grossman et al., 2001; McBride and Feringa, 1992; Nicaise et al., 2013; Nicaise et al., 2012a; Nicaise et al., 2012b; Satkunendrarajah et al., 2016; Yokota et al., 2019). Although immunohistochemical methods enable a broader view of injury-associated changes post-injury (e.g. regional/segmental assessments), they are limited by a lack of specificity to defined cell populations and by their susceptibility to injury-associated changes that do not necessarily correlate with cell loss.
Rat motor neurons caudal to a rubrospinal tract (RST) transection remain viable
2017, NeuroscienceCitation Excerpt :The direct involvement of the gray matter in the above injury models could potentially be attributable to the changes observed in the motor neuron pools caudal to the injury. Contrastively, others have noted no significant loss of motor neurons distal to complete as well as partial transections (McBride and Feringa, 1992; Bjugn et al., 1997) in the rat. These findings corroborate findings in other species.
Multiple sclerosis - candidate mechanisms underlying CNS atrophy
2010, Trends in NeurosciencesCitation Excerpt :In the spinal cord, cell death has been detected in dorsal horn neurons after loss of synaptic input from the dorsal root ganglions [116]. In the ventral horn, however, anterograde transsynaptic degeneration was not observed in alpha motor neurons after spinal-cord transection in rodents [77,78] or in humans [87]. Retrograde degeneration: a degenerative process that starts at the site of axonal lesion and propagates backwards, towards the cell body, eventually leading to cell death.
Effects of hindlimb unloading at early postnatal growth on cell body size in spinal motoneurons innervating soleus muscle of rats
2009, International Journal of Developmental NeuroscienceCitation Excerpt :Despite the adaptation in skeletal muscles to decreased neuromuscular activity and loading levels, the number, cell body size, and oxidative enzyme activity of spinal motoneurons innervating skeletal muscles in adult rats remain stable following hindlimb unloading (Ishihara et al., 1997, 2004). Lack of adaptation in spinal motoneurons to chronic decrease of the neuromuscular activity and loading levels (e.g., spinal cord transection and spinal cord isolation) has been also reported (Donselaar et al., 1986; McBride and Feringa, 1992; Bjugn et al., 1997; Roy et al., 2007). There were no changes in the cell body size or oxidative enzyme activity of motoneurons after spinal cord transaction at a low thoracic and a high sacral level plus bilateral deafferentation between the two transaction sites in cats (Chalmers et al., 1992) or after muscle inactivity in rats induced by chronic tetrodotoxin administration (Seburn et al., 1994).
Differential motor and electrophysiological outcome in rats with mid-thoracic or high lumbar incomplete spinal cord injuries
2006, Brain ResearchCitation Excerpt :Nevertheless, the slight decrease in peripheral muscle responses (M wave) compared to the marked decrease in MEPs in group iL2, the lack of muscle atrophy, and the apparent preservation of spinal cord tissue at L3–L5 segments do not support this explanation to justify the more severe locomotor deficits seen after L2 than in T8 injuries. Regarding the potential impact of thoracic injury on lumbar motoneurons, there are conflicting reports showing either cell death (Eidelberg et al., 1989; Nacimiento et al., 1995) or no effects on cell survival (McBride and Ferringa, 1991; Valero-Cabré et al., 2004). In the present work, the maintenance of the M wave amplitudes in iT8 animals together with the normal histological appearance of L3–L5 spinal segments suggest little, if any, damage.
Effect of spinal cord injury severity on alterations of the H-reflex
2005, Experimental Neurology