ArticleProceedings of the National Academy of Sciences of the United States of America2014
Dystroglycan mediates homeostatic synaptic plasticity at GABAergic synapses.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 100 citations in OpenAlex.
- MiR-30a-5p mediates epileptogenesis in epilepsy models by targeting SOX4 to regulate the Wnt/β-catenin pathway.Epilepsia open · 2026Article
- Neuroligin-2-Dependent Adhesion Defines a Molecular Checkpoint for Inhibitory Synaptic Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- The emerging landscape of brain glycosylation: from molecular complexity to therapeutic potential.Experimental & molecular medicine · 2025Review
- Neuronal hyperexcitability in dystrophin-deficient mdx hippocampal neurons: the importance of interleukin-6 and GABAergic regulation.Scientific reports · 2025Article
- miR218-5p tips the scales.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- microRNA-218-5p coordinates scaling of excitatory and inhibitory synapses during homeostatic synaptic plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Release your inhibitions: The cell biology of GABAergic postsynaptic plasticity.Current opinion in neurobiology · 2025Review
- Alpha-neurexins in health and disease.Frontiers in molecular neuroscience · 2025Review
- The Role of Brain Plasticity in Neuromuscular Disorders: Current Knowledge and Future Prospects.Brain sciences · 2024Review
- GABAergic synaptic scaling is triggered by changes in spiking activity rather than AMPA receptor activation.eLife · 2024Article
- Long-term α5 GABA A receptor negative allosteric modulator treatment reduces NMDAR-mediated neuronal excitation and maintains basal neuronal inhibition.Neuropharmacology · 2023Article
- A combinatorial code of neurexin-3 alternative splicing controls inhibitory synapses via a trans-synaptic dystroglycan signaling loop.Nature communications · 2023Article
- The cell adhesion protein dystroglycan affects the structural remodeling of dendritic spines.Scientific reports · 2022Article
- Fukutin regulates tau phosphorylation and synaptic function: Novel properties of fukutin in neurons.Neuropathology : official journal of the Japanese Society of Neuropathology · 2022Article
- The Yin and Yang of GABAergic and Glutamatergic Synaptic Plasticity: Opposites in Balance by Crosstalking Mechanisms.Frontiers in synaptic neuroscience · 2022Review
- Neurexins and their ligands at inhibitory synapses.Frontiers in synaptic neuroscience · 2022Review
- Extracellular Metalloproteinases in the Plasticity of Excitatory and Inhibitory Synapses.Cells · 2021Review
- Neuronal Dystroglycan regulates postnatal development of CCK/cannabinoid receptor-1 interneurons.Neural development · 2021Article
- Review
- Nitric Oxide Signaling Strengthens Inhibitory Synapses of Cerebellar Molecular Layer Interneurons through a GABARAP-Dependent Mechanism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Dystroglycan (DG), a cell adhesion molecule well known to be essential for skeletal muscle integrity and formation of neuromuscular synapses, is also present at inhibitory synapses in the central nervous system. Mutations that affect DG function not only result in muscular dystrophies, but also in severe cognitive deficits and epilepsy. Here we demonstrate a role of DG during activity-dependent homeostatic regulation of hippocampal inhibitory synapses. Prolonged elevation of neuronal activity up-regulates DG expression and glycosylation, and its localization to inhibitory synapses. Inhibition of protein synthesis prevents the activity-dependent increase in synaptic DG and GABAA receptors (GABAARs), as well as the homeostatic scaling up of GABAergic synaptic transmission. RNAi-mediated knockdown of DG blocks homeostatic scaling up of inhibitory synaptic strength, as does knockdown of like-acetylglucosaminyltransferase (LARGE)--a glycosyltransferase critical for DG function. In contrast, DG is not required for the bicuculline-induced scaling down of excitatory synaptic strength or the tetrodotoxin-induced scaling down of inhibitory synaptic strength. The DG ligand agrin increases GABAergic synaptic strength in a DG-dependent manner that mimics homeostatic scaling up induced by increased activity, indicating that activation of this pathway alone is sufficient to regulate GABAAR trafficking. These data demonstrate that DG is regulated in a physiologically relevant manner in neurons and that DG and its glycosylation are essential for homeostatic plasticity at inhibitory synapses.
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