2023
DOI: 10.1007/s12035-023-03352-5
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Neuronal Store-Operated Calcium Channels

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Cited by 5 publications
(2 citation statements)
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“…Cultured hippocampal neurons prepared from a genetic mouse model of Alzheimer's disease are characterized by a mushroom spine loss that is rescued after the overexpression of TRPC6 channels or after a hyperforin treatment (H. Zhang et al, 2016). Hence, amyloid beta peptide 1-42 (A 42 ) oligomers downregulate the store-operated Ca 2+ entry (SOCE), a prominent neuronal Ca 2+ route (Bouron, 2023). The amplitude of SOCE is however restored when preincubating hippocampal neurons with 0.3 µM hyperforin (Popugaeva et al, 2019).…”
Section: Hyperforin and Alzheimer's Diseasementioning
confidence: 99%
“…Cultured hippocampal neurons prepared from a genetic mouse model of Alzheimer's disease are characterized by a mushroom spine loss that is rescued after the overexpression of TRPC6 channels or after a hyperforin treatment (H. Zhang et al, 2016). Hence, amyloid beta peptide 1-42 (A 42 ) oligomers downregulate the store-operated Ca 2+ entry (SOCE), a prominent neuronal Ca 2+ route (Bouron, 2023). The amplitude of SOCE is however restored when preincubating hippocampal neurons with 0.3 µM hyperforin (Popugaeva et al, 2019).…”
Section: Hyperforin and Alzheimer's Diseasementioning
confidence: 99%
“…In excitable cells, frequent stimulation of voltage-gated and ligand-gated membrane channels allows for multiple modes of Ca 2+ entry possibly rendering STIM/Orai SOCE redundant. However, evidence of SOCE in excitable cells has mounted over the years ( Bouron, 2023 ). Indeed, SOCE was identified in excitable cells well before the molecular mechanism of SOCE through STIM/Orai was elucidated in non-excitable cells ( Emptage et al, 2001 ; Baba et al, 2003 ).…”
mentioning
confidence: 99%