Injury in the spinal cord may produce cell death in the brain

Lee, Bae Hwan; Lee, Kyung Hee; Kim, Un Jeng; Yoon, Do Heum; Sohn, Jong Hee; Choi, Sook Young; Yi, Im-Gap; Park, Yong Gou

doi:10.1016/j.brainres.2004.05.113

Cited by 53 publications

(41 citation statements)

References 23 publications

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“…Furthermore, this idea is supported by observations on CS neurons. In the adult rat, SCI leads to apoptosis in MI (Hains et al, 2003;Lee et al, 2004). However, as mentioned above, in the macaque, the total number of SMI-32 positive cells in layer V of MI remains unchanged , indicating that there occurred no sizeable CS neurons loss.…”

Section: Cell Numbermentioning

confidence: 84%

Fate of rubrospinal neurons after unilateral section of the cervical spinal cord in adult macaque monkeys: Effects of an antibody treatment neutralizing Nogo-A

et al. 2008

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The present study describes in primates the effects of a spinal cord injury on the number and size of the neurons in the magnocellular part of the red nucleus (RNm), the origin of the rubrospinal tract, and evaluates whether a neutralization of Nogo-A reduces the lesionedinduced degenerative processes observed in RNm. Two groups of monkeys were subjected to unilateral section of the spinal cord affecting the rubrospinal tract; one group was subsequently treated with an antibody neutralizing Nogo-A; the second group received a control antibody. Intact animals were also included in the study. Counting neurons stained with a monoclonal antibody recognizing non-phosphorylated epitopes on neurofilaments (SMI-32) indicated that their number in the contralesional RNm was consistently inferior to that in the ipsilesional RNm, in a proportion amounting up to 35%. The lesion also induced shrinkage of the soma of the neurons detected in the contralesional RNm. Infusing an antiNogo-A antibody at the site of the lesion did not increase the proportion of SMI-32 positive rubrospinal neurons in the contralesional RNm nor prevent shrinkage.

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Section: Cell Numbermentioning

confidence: 84%

Fate of rubrospinal neurons after unilateral section of the cervical spinal cord in adult macaque monkeys: Effects of an antibody treatment neutralizing Nogo-A

et al. 2008

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“…Therefore, these cortical changes are unlikely to be due to the axotomy of efferent corticospinal cells (Hains et al, 2003;Lee et al, 2004;Jurkiewicz et al, 2006), to unspecific systemic reactions to the spinal injury, or to the experimental protocol, but are most likely specifically due to the deafferentation. Our result that deafferentation affects cortical slow-wave activity supports the view that this important sleep rhythm is not purely cortical, as usually considered, but is also critically controlled by subcortical structures (Fox and Armstrong-James, 1986;Manjarrez et al, 2002;Crunelli and Hughes, 2010).…”

Section: Pharmacological Block Of the Spinal Cordmentioning

confidence: 99%

Spinal Cord Injury Immediately Changes the State of the Brain

Aguilar¹,

Humanes-Valera²,

et al. 2010

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Spinal cord injury can produce extensive long-term reorganization of the cerebral cortex. Little is known, however, about the sequence of cortical events starting immediately after the lesion. Here we show that a complete thoracic transection of the spinal cord produces immediate functional reorganization in the primary somatosensory cortex of anesthetized rats. Besides the obvious loss of cortical responses to hindpaw stimuli (below the level of the lesion), cortical responses evoked by forepaw stimuli (above the level of the lesion) markedly increase. Importantly, these increased responses correlate with a slower and overall more silent cortical spontaneous activity, representing a switch to a network state of slow-wave activity similar to that observed during slow-wave sleep. The same immediate cortical changes are observed after reversible pharmacological block of spinal cord conduction, but not after sham. We conclude that the deafferentation due to spinal cord injury can immediately (within minutes) change the state of large cortical networks, and that this state change plays a critical role in the early cortical reorganization after spinal cord injury.

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“…Studies suggest that some axotomized neurons are lost, but it has not been clear whether this represents neuronal death or only severe atrophy (Houle and Ye, 1999;Lee et al, 2004;Mori et al, 1997;Novikova et al, 2000Novikova et al, , 2002Takahashi et al, 1999). Several recent publications suggested that a population of injured neurons undergoes apoptosis (Hains et al, 2003;Lee et al, 2004;Takahashi et al, 1999).…”

mentioning

confidence: 97%

Delayed death of identified reticulospinal neurons after spinal cord injury in lampreys

Shifman

Zhang

Selzer

2008

J of Comparative Neurology

122

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There is controversy about whether axotomized neurons undergo death or only severe atrophy after spinal cord injury (SCI) in mammals. Lampreys recover from complete spinal transection, but only about half of the severed spinal-projecting axons regenerate through the site of injury. The fates of the unregenerated neurons remain unknown, and until now death of axotomized spinal-projecting neurons has not been described in the lamprey brain. We now report that in animals allowed to survive for 12 or more weeks after spinal cord transection, several identified reticulospinal (RS) neurons were missing in Nissl-stained or neurofilament-immunostained brain whole mounts. At earlier times, these neurons were swollen and pale in Nissl-stained preparations. Retrograde fluorescent labeling from the site of transection combined with TUNEL histochemistry suggested that neuronal death, including that of the identified RS neurons, began in animals 4 weeks posttransection, reaching a peak at 12-16 weeks. This was not seen in untransected animals. The TUNEL positivity suggests that some cells were dying by apoptosis. Of special interest, among the identified neurons, this delayed cell death was restricted to neurons that at earlier posttransection times have a low probability of regeneration. These data show that SCI induces delayed cell death in lamprey spinal-projecting neurons and suggest that the reason why some neurons are "bad regenerators" is that they are already undergoing apoptotic cell death. Thus protection from apoptosis may be necessary in order to enhance axonal regeneration after SCI.

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Injury in the spinal cord may produce cell death in the brain

Cited by 53 publications

References 23 publications

Fate of rubrospinal neurons after unilateral section of the cervical spinal cord in adult macaque monkeys: Effects of an antibody treatment neutralizing Nogo-A

Fate of rubrospinal neurons after unilateral section of the cervical spinal cord in adult macaque monkeys: Effects of an antibody treatment neutralizing Nogo-A

Spinal Cord Injury Immediately Changes the State of the Brain

Delayed death of identified reticulospinal neurons after spinal cord injury in lampreys

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