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• W2036677209 abstract "The type 1 ryanodine receptor (RyR1) is expressed widely in the brain, with high levels in the cerebellum, hippocampus, and hypothalamus. We have shown that L-type Ca 2+ channels in terminals of hypothalamic magnocellular neurons are coupled to RyRs, as they are in skeletal muscle, allowing voltage-induced Ca 2+ release (VICaR) from internal Ca 2+ stores without Ca 2+ influx. Here we demonstrate that RyR1 plays a role in VICaR in nerve terminals. Furthermore, in heterozygotes from the Ryr1 I4895T/WT (IT/+) mouse line, carrying a knock-in mutation corresponding to one that causes a severe form of human central core disease, VICaR is absent, demonstrating that type 1 RyR mediates VICaR and that these mice have a neuronal phenotype. The absence of VICaR was shown in two ways: first, depolarization in the absence of Ca 2+ influx elicited Ca 2+ syntillas ( scintilla , spark, in a nerve terminal, a SYNaptic structure) in WT, but not in mutant terminals; second, in the presence of extracellular Ca 2+ , IT/+ terminals showed a twofold decrease in global Ca 2+ transients, with no change in plasmalemmal Ca 2+ current. From these studies we draw two conclusions: ( i ) RyR1 plays a role in VICaR in hypothalamic nerve terminals; and ( ii ) a neuronal alteration accompanies the myopathy in IT/+ mice, and, possibly in humans carrying the corresponding RyR1 mutation." @default.
• W2036677209 created "2016-06-24" @default.
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• W2036677209 date "2011-12-27" @default.
• W2036677209 modified "2023-10-18" @default.
• W2036677209 title "Type 1 ryanodine receptor knock-in mutation causing central core disease of skeletal muscle also displays a neuronal phenotype" @default.
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• W2036677209 doi "https://doi.org/10.1073/pnas.1115111108" @default.
• W2036677209 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3258591" @default.
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• W2036677209 hasPublicationYear "2011" @default.
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