ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
The dystrophin Dp186 isoform regulates neurotransmitter release at a central synapse in Drosophila.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
- Optical coherence tomography findings in Duchenne muscular dystrophy.BMC ophthalmology · 2026Article
- Defects of full-length dystrophin trigger retinal neuron damage and synapse alterations by disrupting functional autophagy.Cellular and molecular life sciences : CMLS · 2021Article
- Disrupted-in-Schizophrenia-1 (DISC1) protein disturbs neural function in multiple disease-risk pathways.Human molecular genetics · 2017Article
- Cognitive dysfunction in Duchenne muscular dystrophy: a possible role for neuromodulatory immune molecules.Journal of neurophysiology · 2016Review
- Dystrophin induced cognitive impairment: mechanisms, models and therapeutic strategies.Annals of neurosciences · 2015Review
- Dg-Dys-Syn1 signaling in Drosophila regulates the microRNA profile.BMC cell biology · 2012Article
- Extracellular matrix and its receptors in Drosophila neural development.Developmental neurobiology · 2011Review
- New dystrophin/dystroglycan interactors control neuron behavior in Drosophila eye.BMC neuroscience · 2011Article
- The RhoGAP crossveinless-c interacts with Dystrophin and is required for synaptic homeostasis at the Drosophila neuromuscular junction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Chronic hypoxia impairs muscle function in the Drosophila model of Duchenne's muscular dystrophy (DMD).PloS one · 2010Article
- Article
- The roles of the dystrophin-associated glycoprotein complex at the synapse.Molecular neurobiology · 2010Review
- Flightless flies: Drosophila models of neuromuscular disease.Annals of the New York Academy of Sciences · 2010Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The Dystrophin protein is encoded by a gene that, when mutated in humans, can cause Duchenne muscular dystrophy, a disease characterized by progressive muscle wasting. A number of Duchenne patients also exhibit poorly understood mental retardation, likely associated with loss of a brain-specific isoform. Furthermore, although Dystrophin isoforms and the related Utrophin protein have long been known to localize at synapses, their functions remain essentially unknown. In Drosophila, we find that the CNS-specific Dp186 isoform localizes to the embryonic and larval neuropiles, regions rich in synaptic contacts. In the absence of Dp186, evoked but not spontaneous presynaptic release is significantly enhanced. Increased presynaptic release can be fully rescued to wild-type levels by expression of a Dp186 transgene in the postsynaptic motoneuron, indicating that Dp186 likely regulates a retrograde signaling pathway. Potentiation of synaptic currents in the mutant also occurs when cholinergic transmission is inhibited or in the absence of Glass Bottom Boat (Gbb) or Wishful Thinking (Wit), a TGF-beta ligand and receptor, respectively, both previously implicated in synaptic retrograde signaling. These results are consistent with the possibility that Dp186 modulates other non-Gbb/Wit-dependent retrograde signaling pathways required to maintain normal synaptic physiology.
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Registered trials
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.