ArticleCell death & disease2014
Weakened rate-dependent depression of Hoffmann's reflex and increased motoneuron hyperactivity after motor cortical infarction in mice.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- Ischemic injury to primary motor and premotor cortices is linked to hyperreflexia in mice.Neurobiology of disease · 2026Article
- Application ofActa histochemica et cytochemica · 2026Article
- 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
- Rate-Dependent Depression of the Hoffmann Reflex: Practical Applications in Painful Diabetic Neuropathy.Diabetes & metabolism journal · 2024Review
- MiR-100-5p-rich small extracellular vesicles from activated neuron to aggravate microglial activation and neuronal activity after stroke.Journal of nanobiotechnology · 2024Article
- Combined use of CLP290 and bumetanide alleviates neuropathic pain and its mechanism after spinal cord injury in rats.CNS neuroscience & therapeutics · 2024Article
- Mapping of spastic muscle activity after stroke: difference between passive stretch and active contraction.Journal of neuroengineering and rehabilitation · 2024Article
- Delayed viral vector mediated delivery of neurotrophin-3 improves skilled hindlimb function and stability after thoracic contusion.Experimental neurology · 2023Article
- Harnessing cortical plasticity via gabapentinoid administration promotes recovery after stroke.Brain : a journal of neurology · 2022Article
- The Overexpression of Insulin-Like Growth Factor-1 and Neurotrophin-3 Promote Functional Recovery and Alleviate Spasticity After Spinal Cord Injury.Frontiers in neuroscience · 2022Article
- Changes in muscle-tendon unit length-force characteristics following experimentally induced photothrombotic stroke cannot be explained by changes in muscle belly structure.European journal of applied physiology · 2021Article
- Absence of Subcerebral Projection Neurons Is Beneficial in a Mouse Model of Amyotrophic Lateral Sclerosis.Annals of neurology · 2020Article
- A preclinical model of non-invasive stimulation reduces spinal cord injury initiated spasticity.The Journal of physiology · 2019Article
- Repeated anodal trans-spinal direct current stimulation results in long-term reduction of spasticity in mice with spinal cord injury.The Journal of physiology · 2019Article
- Non-invasive treatment of patients with upper extremity spasticity following stroke using paired trans-spinal and peripheral direct current stimulation.Bioelectronic medicine · 2019Article
- Early movement restriction leads to enduring disorders in muscle and locomotion.Brain pathology (Zurich, Switzerland) · 2018Article
- The H-Reflex as a Biomarker for Spinal Disinhibition in Painful Diabetic Neuropathy.Current diabetes reports · 2018Review
- Mild Intrauterine Hypoperfusion Leads to Lumbar and Cortical Hyperexcitability, Spasticity, and Muscle Dysfunctions in Rats: Implications for Prematurity.Frontiers in neurology · 2018Article
- Hindlimb spasticity after unilateral motor cortex lesion in rats is reduced by contralateral nerve root transfer.Bioscience reports · 2016Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormal reflexes associated with spasticity are considered a major determinant of motor impairments occurring after stroke; however, the mechanisms underlying post-stroke spasticity remain unclear. This may be because of the lack of suitable rodent models for studying spasticity after cortical injuries. Thus, the purpose of the present study was to establish an appropriate post-stroke spasticity mouse model. We induced photothrombotic injury in the rostral and caudal forelimb motor areas of mice and used the rate-dependent depression (RDD) of Hoffmann's reflex (H-reflex) as an indicator of spastic symptoms. To detect motoneuron excitability, we examined c-fos mRNA levels and c-Fos immunoreactivity in affected motoneurons using quantitative real-time reverse transcription PCR and immunohistochemical analysis, respectively. To confirm the validity of our model, we confirmed the effect of the anti-spasticity drug baclofen on H-reflex RDDs 1 week post stroke. We found that 3 days after stroke, the RDD was significantly weakened in the affected muscles of stroke mice compared with sham-operated mice, and this was observed for 8 weeks. The c-fos mRNA levels in affected motoneurons were significantly increased in stroke mice compared with sham-operated mice. Immunohistochemical analysis revealed a significant increase in the number of c-Fos-positive motoneurons in stroke mice compared with sham-operated mice at 1, 2, 4, and 8 weeks after stroke; however, the number of c-Fos-positive motoneurons on both sides of the brain gradually decreased over time. Baclofen treatment resulted in recovery of the weakened RDD at 1 week post stroke. Our findings suggest that this is a viable animal model of post-stroke spasticity.
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