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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Bibliographic Details
Published in:Neuroscience Vol. 229; pp. 77 - 87
Main Authors: Nichols, N.L., Punzo, A.M., Duncan, I.D., Mitchell, G.S., Johnson, R.A.
Format: Journal Article
Language:English
Published: Amsterdam Elsevier Ltd 15.01.2013
Elsevier
Subjects:
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
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
ISSN:0306-4522, 1873-7544, 1873-7544
Online Access:Get full text
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Summary:► 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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ISSN:0306-4522
1873-7544
1873-7544
DOI:10.1016/j.neuroscience.2012.10.066