ArticleNeuroscience letters2015
Abnormally increased surface expression of AMPA receptors in the cerebellum, cortex and striatum of Cln3(-/-) mice.
Article in Neuroscience letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Reversible synaptic deficits in early-stage batten disease.Journal of translational medicine · 2026Article
- Lysosomal alterations and decreased electrophysiological activity in CLN3 disease patient-derived cortical neurons.Disease models & mechanisms · 2022Article
- Autophagy in the Neuronal Ceroid Lipofuscinoses (Batten Disease).Frontiers in cell and developmental biology · 2022Review
- CLN3, at the crossroads of endocytic trafficking.Neuroscience letters · 2021Article
- Ionotropic Glutamate Receptors in Epilepsy: A Review Focusing on AMPA and NMDA Receptors.Biomolecules · 2020Review
- Cross-talk between microglia and neurons regulates HIV latency.PLoS pathogens · 2019Article
- Lack of specificity of antibodies raised against CLN3, the lysosomal/endosomal transmembrane protein mutated in juvenile Batten disease.Bioscience reports · 2017Article
- Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in the CLN3 gene cause a fatal neurodegenerative disorder, juvenile CLN3 disease. Exploring the cause of the motor coordination deficit in the Cln3(-/-) mouse model of the disease we have previously found that attenuation of AMPA receptor activity in 1-month-old Cln3(-/-) mice significantly improves their motor coordination [20]. To elucidate the mechanism of the abnormally increased AMPA receptor function in Cln3(-/-) mice, we examined the surface expression of AMPA receptors using surface cross-linking in brain slices from 1-month-old wild type (WT) and Cln3(-/-) mice. In surface cross-linked brain samples, Western blotting for AMPA receptor subunits revealed significantly increased surface levels of GluA1 and GluA2 in the cerebellum, and of GluA2 in the cortex and striatum of Cln3(-/-) mice as compared to WT mice. Expression levels of the GluA4 subunit were similar in the cerebellum of WT and Cln3(-/-) mice. While intracellular GluA1 levels in the WT and Cln3(-/-) cerebellum or cortex were similar, the intracellular expression of GluA1 in the Cln3(-/-) striatum was decreased to 56% of the WT level. Our results show a prominent increase in AMPA receptor surface expression in the brain of Cln3(-/-) mice and suggest that CLN3 is involved in the regulation of AMPA receptor surface expression.
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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.