ArticleFrontiers in cellular neuroscience2016
Dystrophin Distribution and Expression in Human and Experimental Temporal Lobe Epilepsy.
Article in Frontiers in cellular neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- Epileptic disorders in Becker and Duchenne muscular dystrophies: a systematic review and meta-analysis.Journal of neurology · 2022Pooled it
- Evaluating exon skipping in the central nervous system in Duchenne muscular dystrophy using spatial transcriptomics.iScience · 2026Article
- The Protective Role of Aquaporin 4 (AQP4) in Temporal Lobe Epilepsy: Yes or No?Journal of molecular neuroscience : MN · 2026Review
- Article
- Astrocyte proliferation in the hippocampal dentate gyrus is suppressed across the lifespan of dystrophin-deficient mdx mice.Experimental physiology · 2025Article
- The relative withdrawal of GFAP-An essential component of brain evolution.Frontiers in neuroanatomy · 2025Article
- Astrocytes in human central nervous system diseases: a frontier for new therapies.Signal transduction and targeted therapy · 2023Review
- Specific Dystrophins Selectively Associate with Inhibitory and Excitatory Synapses of the Mouse Cerebellum and their Loss Alters Expression of P2X7 Purinoceptors and Pro-Inflammatory Mediators.Cellular and molecular neurobiology · 2022Article
- Dystrophin in the Neonatal and Adult Rat Intestine.Life (Basel, Switzerland) · 2021Article
- Epigenetic modifications in muscle regeneration and progression of Duchenne muscular dystrophy.Clinical epigenetics · 2021Review
- Principles of Astrogliopathology.Advances in neurobiology · 2021Article
- Dystrophin deficiency leads to dysfunctional glutamate clearance in iPSC derived astrocytes.Translational psychiatry · 2019Article
- Dystrophin is expressed in smooth muscle and afferent nerve fibers in the rat urinary bladder.Muscle & nerve · 2019Article
- Advances in imaging of brain abnormalities in neuromuscular disease.Therapeutic advances in neurological disorders · 2019Review
- Cerebellar synapse properties and cerebellum-dependent motor and non-motor performance inDisease models & mechanisms · 2018Article
- Timing and localization of human dystrophin isoform expression provide insights into the cognitive phenotype of Duchenne muscular dystrophy.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveDystrophin is part of a protein complex that connects the cytoskeleton to the extracellular matrix. In addition to its role in muscle tissue, it functions as an anchoring protein within the central nervous system such as in hippocampus and cerebellum. Its presence in the latter regions is illustrated by the cognitive problems seen in Duchenne Muscular Dystrophy (DMD). Since epilepsy is also supposed to constitute a comorbidity of DMD, it is hypothesized that dystrophin plays a role in neuronal excitability. Here, we aimed to study brain dystrophin distribution and expression in both, human and experimental temporal lobe epilepsy (TLE).
methodRegional and cellular dystrophin distribution was evaluated in both human and rat hippocampi and in rat cerebellar tissue by immunofluorescent colocalization with neuronal (NeuN and calbindin) and glial (GFAP) markers. In addition, hippocampal dystrophin levels were estimated by Western blot analysis in biopsies from TLE patients, post-mortem controls, amygdala kindled (AK)-, and control rats.
resultsDystrophin was expressed in all hippocampal pyramidal subfields and in the molecular-, Purkinje-, and granular cell layer of the cerebellum. In these regions it colocalized with GFAP, suggesting expression in astrocytes such as Bergmann glia (BG) and velate protoplasmic astrocytes. In rat hippocampus and cerebellum there were neither differences in dystrophin positive cell types, nor in the regional dystrophin distribution between AK and control animals. Quantitatively, hippocampal full-length dystrophin (Dp427) levels were about 60% higher in human TLE patients than in post-mortem controls (p < 0.05), whereas the level of the shorter Dp71 isoform did not differ. In contrast, AK animals showed similar dystrophin levels as controls.
conclusionDystrophin is ubiquitously expressed by astrocytes in the human and rat hippocampus and in the rat cerebellum. Hippocampal full-length dystrophin (Dp427) levels are upregulated in human TLE, but not in AK rats, possibly indicating a compensatory mechanism in the chronic epileptic human brain.
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