ArticlePloS one2014
Down-regulation of KCC2 expression and phosphorylation in motoneurons, and increases the number of in primary afferent projections to motoneurons in mice with post-stroke spasticity.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 46 citations in OpenAlex.
- Big conductance calcium-activated potassium channel openers control spasticity without sedation.British journal of pharmacology · 2017Trial
- NMDA Receptor Mediated Mechanisms in the Post-Stroke Brain: From Physiology to Pathology.Biomolecules · 2026Review
- Ischemic injury to primary motor and premotor cortices is linked to hyperreflexia in mice.Neurobiology of disease · 2026Article
- Acupuncture Activates PI3K/Akt Pathway to Promote Spinal Microglial M2 Polarization and Alleviate Spastic Hemiplegia Following Ischemic Stroke.Journal of inflammation research · 2026Article
- Mitochondrial-neuroimmune interfaces in post-stroke spasticity: from acute brain injury to chronic motor phenotypes.Frontiers in neuroscience · 2026Review
- KCC2 phosphorylation dynamics relate to oligomerization during development and after spinal cord injury.Frontiers in molecular neuroscience · 2026Article
- Involvement of the reticulospinal tract in the pathogenesis of spasticity after stroke and spinal cord injury.Frontiers in neuroscience · 2026Review
- Article
- Effect of continuous Ia fibre activity suppression on hyperreflexia-related spasticity and maladaptive synaptic connections in the spinal cord after injury.Scientific reports · 2025Article
- Exercise preconditioning alleviates photothrombotic ischemic stroke in mice by orchestrating neutrophils.Frontiers in physiology · 2025Article
- Continuous Use During Disuse: Mechanisms and Effects of Spontaneous Activity of Unloaded Postural Muscle.International journal of molecular sciences · 2024Review
- Rate-Dependent Depression of the Hoffmann Reflex: Practical Applications in Painful Diabetic Neuropathy.Diabetes & metabolism journal · 2024Review
- Spermidine augments salt stress resilience in rice roots potentially by enhancing OsbZIP73's RNA binding capacity.BMC plant biology · 2024Article
- Oxytocin Exhibits Neuroprotective Effects on Hippocampal Cultures under Severe Oxygen-Glucose Deprivation Conditions.Current issues in molecular biology · 2024Article
- Development of KCC2 therapeutics to treat neurological disorders.Frontiers in molecular neuroscience · 2024Article
- Post-Stroke Spastic Movement Disorder and Botulinum Toxin A Therapy: Early Detection And Early Injection.Annals of rehabilitation medicine · 2023Article
- Ionic Plasticity: Common Mechanistic Underpinnings of Pathology in Spinal Cord Injury and the Brain.Cells · 2022Review
- The Development of Hindlimb Postural Asymmetry Induced by Focal Traumatic Brain Injury Is Not Related to Serotonin 2A/C Receptor Expression in the Spinal Cord.International journal of molecular sciences · 2022Article
- Rate-dependent depression is impaired in amyotrophic lateral sclerosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022Article
- Protective Role of Low Ethanol Administration Following Ischemic Stroke via Recovery of KCC2 and p75Molecular neurobiology · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spasticity obstructs motor function recovery post-stroke, and has been reported to occur in spinal cord injury and electrophysiological studies. The purpose of the present study was to assess spinal cord circuit spasticity in post-stroke mice. At 3, 7, 21, and 42 d after photothrombotic ischemic cortical injury in C57BL/6J mice, we observed decreased rate-dependent depression (RDD) of the Hoffmann reflex (H reflex) in the affected forelimb of mice compared with the limbs of sham mice and the non-affected forelimb. This finding suggests a hyper-excitable stretch reflex in the affected forelimb. We then performed immunohistochemical and western blot analyses to examine the expression of the potassium-chloride cotransporter 2 (KCC2) and phosphorylation of the KCC2 serine residue, 940 (S940), since this is the main chloride extruder that affects neuronal excitability. We also performed immunohistochemical analyses on the number of vesicular glutamate transporter 1 (vGluT1)-positive boutons to count the number of Ia afferent fibers that connect to motoneurons. Western bolts revealed that, compared with sham mice, experimental mice had significantly reduced KCC2 expression at 7 d post-stroke, and dephosphorylated S940 at 3 and 7 d post-stroke in motoneuron plasma membranes. We also observed a lower density of KCC2-positive areas in the plasma membrane of motoneurons at 3 and 7 d post-stroke. However, western blot and immunohistochemical analyses revealed that there were no differences between groups 21 and 42 d post-stroke, respectively. In addition, at 7 and 42 d post-stroke, experimental mice exhibited a significant increase in vGluT1 boutons compared with sham mice. Our findings suggest that both the down-regulation of KCC2 and increases in Ia afferent fibers are involved in post-stroke spasticity.
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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.