ArticleJournal of neuroscience research2010
Altered sensitivity to excitotoxic cell death and glutamate receptor expression between two commonly studied mouse strains.
Article in Journal of neuroscience research, 2010. 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, 15 citations in OpenAlex.
- Lack of specificity of antibodies raised against CLN3, the lysosomal/endosomal transmembrane protein mutated in juvenile Batten disease.Bioscience reports · 2017Article
- Sodium Iodate Produces a Strain-Dependent Retinal Oxidative Stress Response Measured In Vivo Using QUEST MRI.Investigative ophthalmology & visual science · 2017Article
- Decreased sensitivity of palmitoyl protein thioesterase 1-deficient neurons to chemical anoxia.Metabolic brain disease · 2017Article
- Abnormally increased surface expression of AMPA receptors in the cerebellum, cortex and striatum of Cln3(-/-) mice.Neuroscience letters · 2015Article
- Finding the most appropriate mouse model of juvenile CLN3 (Batten) disease for therapeutic studies: the importance of genetic background and gender.Disease models & mechanisms · 2015Article
- Phosphate is not an absolute requirement for the inhibitory effects of cyclosporin A or cyclophilin D deletion on mitochondrial permeability transition.The Biochemical journal · 2012Article
- Strain-specific modifier genes governing craniofacial phenotypes.Birth defects research. Part A, Clinical and molecular teratology · 2012Article
- Altered glutamate receptor function in the cerebellum of the Ppt1-/- mouse, a murine model of infantile neuronal ceroid lipofuscinosis.Journal of neuroscience research · 2012Article
- The effects of aging and genotype on NMDA receptor expression in growth hormone receptor knockout (GHRKO) mice.The journals of gerontology. Series A, Biological sciences and medical sciences · 2011Article
- Altered sensitivity of cerebellar granule cells to glutamate receptor overactivation in the Cln3(Δex7/8)-knock-in mouse model of juvenile neuronal ceroid lipofuscinosis.Neurochemistry international · 2011Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Alterations in glutamatergic synapse function have been implicated in the pathogenesis of many different neurological disorders, including ischemia, epilepsy, Parkinson's disease, Alzheimer's disease, and Huntington's disease. While studying glutamate receptor function in juvenile Batten disease on the C57BL/6J and 129S6/S(v)E(v) mouse backgrounds, we noticed differences unlikely to be due to mutation difference alone. We report here that primary cerebellar granule cell cultures from C57BL/6J mice are more sensitive to N-methyl-D-aspartate (NMDA)-mediated cell death. Moreover, sensitivity to AMPA-mediated excitotoxicity is more variable and is dependent on the treatment conditions and age of the cultures. Glutamate receptor surface expression levels examined in vitro by in situ ELISA and in vivo by Western blot in surface cross-linked cerebellar samples indicated that these differences in sensitivity likely are due to strain-dependent differences in cell surface receptor expression levels. We propose that differences in glutamate receptor expression and in excitotoxic vulnerability should be taken into consideration in the context of characterizing disease models on the C57BL/6J and 129S6/S(v)E(v) mouse backgrounds.
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Registered trials
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