ArticleJournal of neurotrauma2012
Degeneration of phrenic motor neurons induces long-term diaphragm deficits following mid-cervical spinal contusion in mice.
Article in Journal of neurotrauma, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
48 citing papers in PubMed, 72 citations in OpenAlex.
- An update on spinal cord injury and diaphragm neuromotor control.Expert review of respiratory medicine · 2025Review
- Respiratory neuropathology in spinocerebellar ataxia type 7.JCI insight · 2024Article
- Ampakines increase diaphragm activation following mid-cervical contusion injury in rats.Experimental neurology · 2024Article
- Article
- Review
- Changes in respiratory structure and function after traumatic cervical spinal cord injury: observations from spinal cord and brain.Frontiers in neurology · 2023Review
- Neuro-respiratory pathology in spinocerebellar ataxia.Journal of the neurological sciences · 2022Review
- Respiratory plasticity following spinal cord injury: perspectives from mouse to man.Neural regeneration research · 2022Review
- SV2A PET Imaging Is a Noninvasive Marker for the Detection of Spinal Damage in Experimental Models of Spinal Cord Injury.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2022Article
- The extra-cerebellar effects of spinocerebellar ataxia type 1 (SCA1): looking beyond the cerebellum.Cellular and molecular life sciences : CMLS · 2022Review
- Diaphragmatic Activity and Respiratory Function Following C3 or C6 Unilateral Spinal Cord Contusion in Mice.Biology · 2022Article
- Phrenic motor neuron survival below cervical spinal cord hemisection.Experimental neurology · 2021Article
- Respiratory dysfunction in a mouse model of spinocerebellar ataxia type 7.Disease models & mechanisms · 2021Article
- Cystine-glutamate antiporter deletion accelerates motor recovery and improves histological outcomes following spinal cord injury in mice.Scientific reports · 2021Article
- LAR inhibitory peptide promotes recovery of diaphragm function and multiple forms of respiratory neural circuit plasticity after cervical spinal cord injury.Neurobiology of disease · 2021Article
- Respiratory Training and Plasticity After Cervical Spinal Cord Injury.Frontiers in cellular neuroscience · 2021Review
- Hyperbaric Oxygen Treatment Following Mid-Cervical Spinal Cord Injury Preserves Diaphragm Muscle Function.International journal of molecular sciences · 2020Article
- Spinal cord injury and diaphragm neuromotor control.Expert review of respiratory medicine · 2020Review
- Combination of a Gellan Gum-Based Hydrogel With Cell Therapy for the Treatment of Cervical Spinal Cord Injury.Frontiers in bioengineering and biotechnology · 2020Article
- Is Innervation of the Neuromuscular Junction at the Diaphragm Modulated by sGC/cGMP Signaling?Frontiers in physiology · 2020Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A primary cause of morbidity and mortality following cervical spinal cord injury (SCI) is respiratory compromise, regardless of the level of trauma. In particular, SCI at mid-cervical regions targets degeneration of both descending bulbospinal respiratory axons and cell bodies of phrenic motor neurons, resulting in deficits in the function of the diaphragm, the primary muscle of inspiration. Contusion-type trauma to the cervical spinal cord is one of the most common forms of human SCI; however, few studies have evaluated mid-cervical contusion in animal models or characterized consequent histopathological and functional effects of degeneration of phrenic motor neuron-diaphragm circuitry. We have generated a mouse model of cervical contusion SCI that unilaterally targets both C4 and C5 levels, the location of the phrenic motor neuron pool, and have examined histological and functional outcomes for up to 6 weeks post-injury. We report that phrenic motor neuron loss in cervical spinal cord, phrenic nerve axonal degeneration, and denervation at diaphragm neuromuscular junctions (NMJ) resulted in compromised ipsilateral diaphragm function, as demonstrated by persistent reduction in diaphragm compound muscle action potential amplitudes following phrenic nerve stimulation and abnormalities in spontaneous diaphragm electromyography (EMG) recordings. This injury paradigm is reproducible, does not require ventilatory assistance, and provides proof-of-principle that generation of unilateral cervical contusion is a feasible strategy for modeling diaphragmatic/respiratory deficits in mice. This study and its accompanying analyses pave the way for using transgenic mouse technology to explore the function of specific genes in the pathophysiology of phrenic motor neuron degeneration and respiratory dysfunction following cervical SCI.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.