ArticleFrontiers in cellular neuroscience2022
Altered Synaptic Transmission and Excitability of Cerebellar Nuclear Neurons in a Mouse Model of Duchenne Muscular Dystrophy.
Article in Frontiers in cellular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Anti-Inflammatory and Synaptic Protective Effects of TNF-α Inactivation in the MDX Mouse Model.Current issues in molecular biology · 2026Article
- Central Neurophysiological Alterations in Dystrophic mdx Mice Correlate With Reduced Hippocampal Levels of the Endogenous NMDA Receptor Ligand D-Aspartate.Journal of neurochemistry · 2025Article
- Understanding Duchenne muscular dystrophy-associated brain pathology.Disease models & mechanisms · 2025Review
- The role of dystrophin isoforms and interactors in the brain.Brain : a journal of neurology · 2025Review
- Spatiotemporal diversity in molecular and functional abnormalities in the mdx dystrophic brain.Molecular medicine (Cambridge, Mass.) · 2025Article
- Duchenne muscular dystrophy: recent insights in brain related comorbidities.Nature communications · 2025Review
- The Role of Brain Plasticity in Neuromuscular Disorders: Current Knowledge and Future Prospects.Brain sciences · 2024Review
- Exome sequencing reveals neurodevelopmental genes in simplex consanguineous Iranian families with syndromic autism.BMC medical genomics · 2024Article
- Dmd mdx mice have defective oligodendrogenesis, delayed myelin compaction and persistent hypomyelination.Disease models & mechanisms · 2024Article
- Primary mouse myoblast metabotropic purinoceptor profiles and calcium signalling differ with their muscle origin and are altered in mdx dystrophinopathy.Scientific reports · 2023Article
- Blockade of Cholecystokinin Type 2 Receptors Prevents the Onset of Vincristine-Induced Neuropathy in Mice.Pharmaceutics · 2022Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is generally regarded as a muscle-wasting disease. However, human patients and animal models of DMD also frequently display non-progressive cognitive deficits and high comorbidity with neurodevelopmental disorders, suggesting impaired central processing. Previous studies have identified the cerebellar circuit, and aberrant inhibitory transmission in Purkinje cells, in particular, as a potential site of dysfunction in the central nervous system (CNS). In this work, we investigate potential dysfunction in the output of the cerebellum, downstream of Purkinje cell (PC) activity. We examined synaptic transmission and firing behavior of excitatory projection neurons of the cerebellar nuclei, the primary output of the cerebellar circuit, in juvenile wild-type and
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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.