ArticlePloS one2014
Aberrant location of inhibitory synaptic marker proteins in the hippocampus of dystrophin-deficient mice: implications for cognitive impairment in duchenne muscular dystrophy.
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 19 papers.
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Who cites it
19 citing papers in PubMed, 36 citations in OpenAlex.
- Deficient Astrocyte Homeostatic Support Contributes to Brain Impairment in Duchenne Muscular Dystrophy.Neurochemical research · 2025Review
- Neuronal hyperexcitability in dystrophin-deficient mdx hippocampal neurons: the importance of interleukin-6 and GABAergic regulation.Scientific reports · 2025Article
- 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
- Article
- Abnormal Expression of Synaptic and Extrasynaptic GABAInternational journal of molecular sciences · 2022Article
- 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
- Disrupted Calcium Homeostasis in Duchenne Muscular Dystrophy: A Common Mechanism behind Diverse Consequences.International journal of molecular sciences · 2021Review
- Dystroglycan Mediates Clustering of Essential GABAergic Components in Cerebellar Purkinje Cells.Frontiers in molecular neuroscience · 2020Article
- Characterization of brain dystrophins absence and impact in dystrophin-deficient Dmdmdx rat model.PloS one · 2020Article
- Article
- Neuronal Dystroglycan Is Necessary for Formation and Maintenance of Functional CCK-Positive Basket Cell Terminals on Pyramidal Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Glycan susceptibility factors in autism spectrum disorders.Molecular aspects of medicine · 2016Review
- Reversal of neurobehavioral social deficits in dystrophic mice using inhibitors of phosphodiesterases PDE5A and PDE9A.Translational psychiatry · 2016Article
- Cognitive dysfunction in Duchenne muscular dystrophy: a possible role for neuromodulatory immune molecules.Journal of neurophysiology · 2016Review
- Current Translational Research and Murine Models For Duchenne Muscular Dystrophy.Journal of neuromuscular diseases · 2016Review
- Dystrophin: The dead calm of a dogma.Rare diseases (Austin, Tex.) · 2016Article
- P2RX7 purinoceptor: a therapeutic target for ameliorating the symptoms of duchenne muscular dystrophy.PLoS medicine · 2015Article
- Altered social behavior and ultrasonic communication in the dystrophin-deficient mdx mouse model of Duchenne muscular dystrophy.Molecular autism · 2015Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne muscular dystrophy (DMD) is a neuromuscular disease that arises from mutations in the dystrophin-encoding gene. Apart from muscle pathology, cognitive impairment, primarily of developmental origin, is also a significant component of the disorder. Convergent lines of evidence point to an important role for dystrophin in regulating the molecular machinery of central synapses. The clustering of neurotransmitter receptors at inhibitory synapses, thus impacting on synaptic transmission, is of particular significance. However, less is known about the role of dystrophin in influencing the precise expression patterns of proteins located within the pre- and postsynaptic elements of inhibitory synapses. To this end, we exploited molecular markers of inhibitory synapses, interneurons and dystrophin-deficient mouse models to explore the role of dystrophin in determining the stereotypical patterning of inhibitory connectivity within the cellular networks of the hippocampus CA1 region. In tissue from wild-type (WT) mice, immunoreactivity of neuroligin2 (NL2), an adhesion molecule expressed exclusively in postsynaptic elements of inhibitory synapses, and the vesicular GABA transporter (VGAT), a marker of GABAergic presynaptic elements, were predictably enriched in strata pyramidale and lacunosum moleculare. In acute contrast, NL2 and VGAT immunoreactivity was relatively evenly distributed across all CA1 layers in dystrophin-deficient mice. Similar changes were evident with the cannabinoid receptor 1, vesicular glutamate transporter 3, parvalbumin, somatostatin and the GABAA receptor alpha1 subunit. The data show that in the absence of dystrophin, there is a rearrangement of the molecular machinery, which underlies the precise spatio-temporal pattern of GABAergic synaptic transmission within the CA1 sub-field of the hippocampus.
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