ArticleNeurobiology of disease2018
A third copy of the Down syndrome cell adhesion molecule (Dscam) causes synaptic and locomotor dysfunction in Drosophila.
Article in Neurobiology of disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Increased endothelial sclerostin caused by elevated DSCAM mediates multiple trisomy 21 phenotypes.The Journal of clinical investigation · 2024Article
- The role of Down syndrome cell adhesion molecule in Down syndrome.Medical review (2021) · 2024Review
- Article
- DSCAM gene triplication causes excessive GABAergic synapses in the neocortex in Down syndrome mouse models.PLoS biology · 2023Article
- Dscam1 overexpression impairs the function of the gut nervous system in Drosophila.Developmental dynamics : an official publication of the American Association of Anatomists · 2023Article
- Memory consolidation in honey bees is enhanced by down-regulation ofFrontiers in molecular neuroscience · 2023Article
- Dysfunction of NMDA receptors in neuronal models of an autism spectrum disorder patient with a DSCAM mutation and in Dscam-knockout mice.Molecular psychiatry · 2021Article
- Role of DSCAM in the Development of Neural Control of Movement and Locomotion.International journal of molecular sciences · 2021Review
- Neuronal overexpression of Alzheimer's disease and Down's syndrome associated DYRK1A/minibrain gene alters motor decline, neurodegeneration and synaptic plasticity in Drosophila.Neurobiology of disease · 2019Article
- Nuclear import of the DSCAM-cytoplasmic domain drives signaling capable of inhibiting synapse formation.The EMBO journal · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Down syndrome (DS) is caused by triplication of chromosome 21 (HSA21). It is characterised by intellectual disability and impaired motor coordination that arise from changes in brain volume, structure and function. However, the contribution of each HSA21 gene to these various phenotypes and to the causal alterations in neuronal and synaptic structure and function are largely unknown. Here we have investigated the effect of overexpression of the HSA21 gene DSCAM (Down syndrome cell adhesion molecule), on glutamatergic synaptic transmission and motor coordination, using Drosophila expressing three copies of Dscam1. Electrophysiological recordings of miniature and evoked excitatory junction potentials at the glutamatergic neuromuscular junction of Drosophila larvae showed that the extra copy of Dscam1 changed the properties of spontaneous and electrically-evoked transmitter release and strengthened short-term synaptic depression during high-frequency firing of the motor nerve. Behavioural analyses uncovered impaired locomotor coordination despite preserved gross motor function. This work identifies DSCAM as a candidate causative gene in DS that is sufficient to modify synaptic transmission and synaptic plasticity and cause a DS behavioural phenotype.
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