ArticleExperimental neurology2013
Motoneuron BDNF/TrkB signaling enhances functional recovery after cervical spinal cord injury.
Article in Experimental neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.
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Who cites it
85 citing papers in PubMed, 1 synthesis or guideline pooled it, 109 citations in OpenAlex.
- Comparing the Efficacy and Safety of Cell Transplantation for Spinal Cord Injury: A Systematic Review and Bayesian Network Meta-Analysis.Frontiers in cellular neuroscience · 2022Pooled it
- Circadian clock protein Bmal1 regulates respiratory motor plasticity in male rats.Function (Oxford, England) · 2026Article
- Size-dependent alterations in phrenic motor neuron perineuronal nets following cervical spinal hemisection.Journal of neurophysiology · 2026Article
- Vagal suppression of diurnal variations in acute intermittent hypoxia-induced phrenic long-term facilitation.Journal of neurophysiology · 2026Article
- Motor Neuron Size-Dependent Differences in mRNA Expression of Tropomyosin-Related Kinase Receptor B in Adult Rats.Journal of neurochemistry · 2026Article
- Impact of upper cervical spinal cord hemisection on diaphragm neuromotor control.Journal of neurophysiology · 2025Article
- The role of Genipin crosslinked extracellular matrix loaded bFGF in the repair of peripheral nerve injury.BMC biotechnology · 2025Article
- An update on spinal cord injury and diaphragm neuromotor control.Expert review of respiratory medicine · 2025Review
- BDNF-TrkB Signaling Pathway in Spinal Cord Injury: Insights and Implications.Molecular neurobiology · 2025Review
- AMPA receptors play an important role in the biological consequences of spinal cord injury: Implications for AMPA receptor modulators for therapeutic benefit.Biochemical pharmacology · 2024Review
- Inactivity-induced phrenic motor facilitation requires PKCζ activity within phrenic motor neurons.Journal of neurophysiology · 2024Article
- Cervical spinal cord hemisection impacts sigh and the respiratory reset in male rats.Physiological reports · 2024Article
- Traumatic brain injury: molecular biomarkers, genetics, secondary consequences, and medical management.Frontiers in neuroscience · 2024Review
- Routine hypercapnic challenge after cervical spinal hemisection affects the size of phrenic motoneurons.Scientific reports · 2023Article
- Chemogenetic inhibition of TrkB signalling reduces phrenic motor neuron survival and size.Molecular and cellular neurosciences · 2023Article
- Novel regenerative drug, SPG302 promotes functional recovery of diaphragm muscle activity after cervical spinal cord injury.The Journal of physiology · 2023Article
- Review
- Swimming and L-arginine loaded chitosan nanoparticles ameliorates aging-induced neuron atrophy, autophagy marker LC3, GABA and BDNF-TrkB pathway in the spinal cord of rats.Pflugers Archiv : European journal of physiology · 2023Article
- Brain-Derived Neurotrophic Factor Is Indispensable to Continence Recovery after a Dual Nerve and Muscle Childbirth Injury Model.International journal of molecular sciences · 2023Article
- Targeting drug or gene delivery to the phrenic motoneuron pool.Journal of neurophysiology · 2023Review
25 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
A C2 cervical spinal cord hemisection (SH) interrupts descending inspiratory-related drive to phrenic motoneurons located between C3 and C5 in rats, paralyzing the ipsilateral hemidiaphragm muscle. There is gradual recovery of rhythmic diaphragm muscle activity ipsilateral to cervical spinal cord injury over time, consistent with neuroplasticity and strengthening of spared, contralateral descending premotor input to phrenic motoneurons. Brain-derived neurotrophic factor (BDNF) signaling through the tropomyosin related kinase receptor subtype B (TrkB) plays an important role in neuroplasticity following spinal cord injury. We hypothesized that 1) increasing BDNF/TrkB signaling at the level of the phrenic motoneuron pool by intrathecal BDNF delivery enhances functional recovery of rhythmic diaphragm activity after SH, and 2) inhibiting BDNF/TrkB signaling by quenching endogenous neurotrophins with the soluble fusion protein TrkB-Fc or by knocking down TrkB receptor expression in phrenic motoneurons using intrapleurally-delivered siRNA impairs functional recovery after SH. Diaphragm EMG electrodes were implanted bilaterally to verify complete hemisection at the time of SH and 3days post-SH. After SH surgery in adult rats, an intrathecal catheter was placed at C4 to chronically infuse BDNF or TrkB-Fc using an implanted mini-osmotic pump. At 14days post-SH, all intrathecal BDNF treated rats (n=9) displayed recovery of ipsilateral hemidiaphragm EMG activity, compared to 3 out of 8 untreated SH rats (p<0.01). During eupnea, BDNF treated rats exhibited 76±17% of pre-SH root mean squared EMG vs. only 5±3% in untreated SH rats (p<0.01). In contrast, quenching endogenous BDNF with intrathecal TrkB-Fc treatment completely prevented functional recovery up to 14days post-SH (n=7). Immunoreactivity of the transcription factor cAMP response element-binding protein (CREB), a downstream effector of TrkB signaling, increased in phrenic motoneurons following BDNF treatment (n=6) compared to artificial cerebrospinal fluid treatment (n=6; p<0.001). Intrapleural injections of non-sense or TrkB siRNA were administered after SH to specifically target phrenic motoneurons. At 14days post-SH, none out of 9 TrkB siRNA treated rats displayed functional recovery compared to 5 out of 9 non-sense siRNA treated rats. These results indicate that BDNF/TrkB signaling in phrenic motoneuron pool plays a critical role in functional recovery after cervical spinal cord injury.
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