Cervical spinal demyelination with ethidium bromide impairs respiratory (phrenic) activity and forelimb motor behavior in rats
► Spinal ethidium bromide injections produced transient dorsolateral demyelination. ► Ventilation did not change with ethidium bromide (EB) demyelination. ► Ipsilateral phrenic nerve amplitude was transiently reduced post-EB. ► Ipsilateral limb function was continually impaired post-EB. ► EB provide...
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| Vydané v: | Neuroscience Ročník 229; s. 77 - 87 |
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| Hlavní autori: | , , , , |
| Médium: | Journal Article |
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Elsevier Ltd
15.01.2013
Elsevier |
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| ISSN: | 0306-4522, 1873-7544, 1873-7544 |
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| Abstract | ► Spinal ethidium bromide injections produced transient dorsolateral demyelination. ► Ventilation did not change with ethidium bromide (EB) demyelination. ► Ipsilateral phrenic nerve amplitude was transiently reduced post-EB. ► Ipsilateral limb function was continually impaired post-EB. ► EB provides a reversible demyelination model to study compensatory motor plasticity.
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 functions are impaired in a rat model of focal dorsolateral spinal demyelination (ethidium bromide, EB). Ventilation, phrenic nerve activity and horizontal ladder walking were performed 7–14days post-C2 injection of EB or vehicle (SHAM). EB caused dorsolateral demyelination at C2–C3 followed by significant spontaneous remyelination at 14days post-EB. Although ventilation did not differ between groups, ipsilateral integrated phrenic nerve burst amplitude was significantly reduced versus SHAM during chemoreceptor activation at 7days post-EB but recovered by 14days. The ratio of ipsi- to contralateral phrenic nerve amplitude correlated with cross-sectional lesion area. This ratio was significantly reduced 7days post-EB versus SHAM during baseline conditions, and versus SHAM and 14-day groups during chemoreceptor activation. Limb function ipsilateral to EB was impaired 7days post-EB and partially recovered by 14days 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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| AbstractList | Highlights ► Spinal ethidium bromide injections produced transient dorsolateral demyelination. ► Ventilation did not change with ethidium bromide (EB) demyelination. ► Ipsilateral phrenic nerve amplitude was transiently reduced post-EB. ► Ipsilateral limb function was continually impaired post-EB. ► EB provides a reversible demyelination model to study compensatory motor plasticity. 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. ► Spinal ethidium bromide injections produced transient dorsolateral demyelination. ► Ventilation did not change with ethidium bromide (EB) demyelination. ► Ipsilateral phrenic nerve amplitude was transiently reduced post-EB. ► Ipsilateral limb function was continually impaired post-EB. ► EB provides a reversible demyelination model to study compensatory motor plasticity. 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 functions are impaired in a rat model of focal dorsolateral spinal demyelination (ethidium bromide, EB). Ventilation, phrenic nerve activity and horizontal ladder walking were performed 7–14days post-C2 injection of EB or vehicle (SHAM). EB caused dorsolateral demyelination at C2–C3 followed by significant spontaneous remyelination at 14days post-EB. Although ventilation did not differ between groups, ipsilateral integrated phrenic nerve burst amplitude was significantly reduced versus SHAM during chemoreceptor activation at 7days post-EB but recovered by 14days. The ratio of ipsi- to contralateral phrenic nerve amplitude correlated with cross-sectional lesion area. This ratio was significantly reduced 7days post-EB versus SHAM during baseline conditions, and versus SHAM and 14-day groups during chemoreceptor activation. Limb function ipsilateral to EB was impaired 7days post-EB and partially recovered by 14days 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. 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 functions 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 significant 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.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 functions 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 significant 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. 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 functions 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 significant 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. |
| Author | Punzo, A.M. Duncan, I.D. Mitchell, G.S. Johnson, R.A. Nichols, N.L. |
| AuthorAffiliation | c Department of Medical Sciences, University of Wisconsin, Madison, WI 53706 b Department of Surgical Sciences, University of Wisconsin, Madison, WI 53706 a Department of Comparative Biosciences, University of Wisconsin, Madison, WI 53706 |
| AuthorAffiliation_xml | – name: b Department of Surgical Sciences, University of Wisconsin, Madison, WI 53706 – name: a Department of Comparative Biosciences, University of Wisconsin, Madison, WI 53706 – name: c Department of Medical Sciences, University of Wisconsin, Madison, WI 53706 |
| Author_xml | – sequence: 1 givenname: N.L. surname: Nichols fullname: Nichols, N.L. email: nichols.36@wright.edu organization: Department of Comparative Biosciences, University of Wisconsin, Madison, WI 53706, United States – sequence: 2 givenname: A.M. surname: Punzo fullname: Punzo, A.M. email: ahayes3@svm.vetmed.wisc.edu organization: Department of Surgical Sciences, University of Wisconsin, Madison, WI 53706, United States – sequence: 3 givenname: I.D. surname: Duncan fullname: Duncan, I.D. email: duncani@svm.vetmed.wisc.edu organization: Department of Medical Sciences, University of Wisconsin, Madison, WI 53706, United States – sequence: 4 givenname: G.S. surname: Mitchell fullname: Mitchell, G.S. email: mitchell@svm.vetmed.wisc.edu organization: Department of Comparative Biosciences, University of Wisconsin, Madison, WI 53706, United States – sequence: 5 givenname: R.A. surname: Johnson fullname: Johnson, R.A. email: pipob@svm.vetmed.wisc.edu organization: Department of Surgical Sciences, University of Wisconsin, Madison, WI 53706, United States |
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| Keywords | PBS myelin Spinal cord V˙E VT/TI f FIO2 ventilation CNS PETCO2 PaO2 ANOVA TI phrenic nerve amplitude motor function LSD EB VT compensatory plasticity FIO 2 phosphate-buffered saline V T inspiratory fraction of oxygen analysis of variance mean inspiratory flow tidal volume P ETCO 2 arterial partial pressure of oxygen V ˙ E inspiratory time PaO 2 breathing frequency Fisher’s least significant difference V T/ T I central nervous system minute ventilation (the product of breathing frequency and tidal volume) partial pressure of end-tidal carbon dioxide T I ethidium bromide Rat Myelin Rodentia Central nervous system Respiratory system Motor control Vertebrata Mammalia Phrenic nerve Demyelination Animal Plasticity Upper limb Behavior Pulmonary ventilation Respiration Forelimb |
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| Snippet | ► Spinal ethidium bromide injections produced transient dorsolateral demyelination. ► Ventilation did not change with ethidium bromide (EB) demyelination. ►... Highlights ► Spinal ethidium bromide injections produced transient dorsolateral demyelination. ► Ventilation did not change with ethidium bromide (EB)... Although respiratory complications are a major cause of morbidity/mortality in many neural injuries or diseases, little is known concerning mechanisms whereby... |
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| SubjectTerms | Animals Biological and medical sciences Cervical Vertebrae compensatory plasticity Demyelinating Diseases - chemically induced Demyelinating Diseases - physiopathology Diaphragm - innervation Diaphragm - physiopathology Ethidium Forelimb - physiology Fundamental and applied biological sciences. Psychology Motor Activity - physiology Motor control and motor pathways. Reflexes. Control centers of vegetative functions. Vestibular system and equilibration motor function Motor Neurons - physiology myelin Neurology Phrenic Nerve - physiopathology phrenic nerve amplitude Rats Rats, Sprague-Dawley Respiration Spinal cord Spinal Cord - physiopathology ventilation Vertebrates: nervous system and sense organs Walking - physiology |
| Title | Cervical spinal demyelination with ethidium bromide impairs respiratory (phrenic) activity and forelimb motor behavior in rats |
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