OSP-Immunofluorescent remyelinating oligodendrocytes in the brainstem of toxically-demyelinated Wistar rats

Sallis, Eliza Simone Viégas; Mazzanti, Cinthia M.; Mazzantí, Alexandre; Arroteia, Kélen Fabíola; Fustigatto, Rafael; Pelizzari, Charles; Rodrigues, Aline; Graça, Dominguita Lühers

doi:10.1590/s0004-282x2006000200013

Cited by 10 publications

(6 citation statements)

References 17 publications

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“…2A–C). These results are in agreement with previous works regarding the EB gliotoxic model (Bondan et al, 2000; Bondan et al, 2003; Graça et al, 2001; Salis et al, 2006; Mazzanti et al, 2006a,b, 2007; Spanevello et al, 2006). In Vit E and ebselen treated rats, lesions induced by EB were smaller suggesting that these compounds somehow interfered in the development of the lesions.…”

Section: Discussionsupporting

confidence: 93%

Pre‐treatment with ebselen and vitamin E modulate acetylcholinesterase activity: interaction with demyelinating agents

Mazzanti

Spanevello

Ahmed

et al. 2008

Intl J of Devlp Neuroscience

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The ethidium bromide (EB) demyelinating model was associated with vitamin E (Vit E) and ebselen (Ebs) treatment to evaluate acetylcholinesterase (AChE) activity in the striatum (ST), hippocampus (HP), cerebral cortex (CC) and erythrocytes. Rats were divided into seven groups: I-Control (saline), II-(canola); III-(Ebs), IV-(Vit E); V-(EB); VI-(EB+Ebs) and VII-(EB+Vit E). At 3 days after the EB injection, AChE activity in the CC and HC was significantly reduced in groups III, IV, V, VI and VII (p<0.05) and in the ST it was reduced in groups III and V (p<0.05) when compared to the control group. At 21 days after the EB injection, AChE activity in the CC was significantly reduced in groups III, IV and V, while in groups VI and VII a significant increase was observed when compared to the control group. In the HC and ST, AChE activity was significantly reduced in groups V, VI and VII when compared to the control group (p<0.05). In the erythrocytes, at 3 days after the EB injection, AChE activity was significantly reduced in groups III, IV, V, VI and VII and at 21 days there was a significant reduction only in groups VI and VII (p<0.05) when compared to the control group. In conclusion, this study demonstrated that Ebs and Vit E interfere with the cholinergic neurotransmission by altering AChE activity in the different brain regions and in the erythrocytes. Furthermore, treatment with Vit E and Ebs protected against the demyelination lesion caused by EB. In this context, we can suggest that ebselen and Vit E should be considered potential therapeutics and scientific tools to be investigated in brain disorders associated with demyelinating events.

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Section: Discussionsupporting

confidence: 93%

Pre‐treatment with ebselen and vitamin E modulate acetylcholinesterase activity: interaction with demyelinating agents

Mazzanti

Spanevello

Ahmed

et al. 2008

Intl J of Devlp Neuroscience

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“…EB-induced demyelination is reversible; Schwann cells are present by 7 days post-injection and extensive spontaneous remyelination is observed 2 weeks post-EB (Blakemore, 1982; Graça and Blakemore, 1986; Sallis et al, 2006; Bondan et al, 2010; Nichols et al, 2012). Consistent with the time course of spontaneous remyelination, phrenic nerve activity returns to pre-injection levels by 14 days, providing a model to study the reversibility of endogenous compensatory mechanisms (Nichols et al, 2012).…”

Section: Rodent Models Of Respiratory Compromise In Neurological Dmentioning

confidence: 99%

Common mechanisms of compensatory respiratory plasticity in spinal neurological disorders

Johnson

Mitchell

2013

Respiratory Physiology & Neurobiology

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In many neurological disorders that disrupt spinal function and compromise breathing (e.g. ALS, cervical spinal injury, MS), patients often maintain ventilatory capacity well after the onset of severe CNS pathology. In progressive neurodegenerative diseases, patients ultimately reach a point where compensation is no longer possible, leading to catastrophic ventilatory failure. In this brief review, we consider evidence that common mechanisms of compensatory respiratory plasticity preserve breathing capacity in diverse clinical disorders, despite the onset of severe pathology (e.g. respiratory motor neuron denervation and/or death). We propose that a suite of mechanisms, operating at distinct sites in the respiratory control system, underlies compensatory respiratory plasticity, including: 1) increased (descending) central respiratory drive, 2) motor neuron plasticity, 3) plasticity at the neuromuscular junction or spared respiratory motor neurons, and 4) shifts in the balance from more to less severely compromised respiratory muscles. To establish this framework, we contrast three rodent models of neural dysfunction, each posing unique problems for the generation of adequate inspiratory motor output: 1) respiratory motor neuron death, 2) de- or dysmyelination of cervical spinal pathways, and 3) cervical spinal cord injury, a neuropathology with components of demyelination and motor neuron death. Through this contrast, we hope to understand the multilayered strategies used to “fight” for adequate breathing in the face of mounting pathology.

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“…However, remyelination occurs spontaneously; Schwann cells are present within 7 days and extensive remyelination is observed by 13 days (Blakemore, 1982; Graça and Blakemore, 1986; Sallis et al, 2006; Bondan et al, 2010). Our results are consistent with these earlier reports as spinal tracts were demyelinated at 7 days post-EB, with remyelination observed at 14 days.…”

Section: Discussionmentioning

confidence: 99%

Cervical spinal demyelination with ethidium bromide impairs respiratory (phrenic) activity and forelimb motor behavior in rats

et al. 2013

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Although respiratory complications are a major cause of morbidity/mortality in many neural injuries or diseases, little is known concerning mechanisms whereby deficient myelin impairs breathing, or how patients compensate for such changes. Here, we tested the hypothesis that respiratory and forelimb motor function are impaired in a rat model of focal dorsolateral spinal demyelination (ethidium bromide, EB). Ventilation, phrenic nerve activity and horizontal ladder walking were performed 7-14 days post-C2 injection of EB or vehicle (SHAM). EB caused dorsolateral demyelination at C2-C3 followed by signficant spontaneous remyelination at 14 days post-EB. Although ventilation did not differ between groups, ipsilateral integrated phrenic nerve burst amplitude was significantly reduced versus SHAM during chemoreceptor activation at 7 days post-EB but recovered by 14 days. The ratio of ipsi- to contralateral phrenic nerve amplitude correlated with cross-sectional lesion area. This ratio was significantly reduced 7 days post-EB versus SHAM during baseline conditions, and versus SHAM and 14 day groups during chemoreceptor activation. Limb function ipsilateral to EB was impaired 7 days post-EB and partially recovered by 14 days post-EB. EB provides a reversible model of focal, spinal demyelination, and may be a useful model to study mechanisms of functional impairment and recovery via motor plasticity, or the efficacy of new therapeutic interventions to reduce severity or duration of disease.

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OSP-Immunofluorescent remyelinating oligodendrocytes in the brainstem of toxically-demyelinated Wistar rats

Cited by 10 publications

References 17 publications

Pre‐treatment with ebselen and vitamin E modulate acetylcholinesterase activity: interaction with demyelinating agents

Pre‐treatment with ebselen and vitamin E modulate acetylcholinesterase activity: interaction with demyelinating agents

Common mechanisms of compensatory respiratory plasticity in spinal neurological disorders

Cervical spinal demyelination with ethidium bromide impairs respiratory (phrenic) activity and forelimb motor behavior in rats

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