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• W2969156715 endingPage "101676" @default.
• W2969156715 startingPage "101676" @default.
• W2969156715 abstract "Angelman syndrome (AS) is a neurodevelopmental disorder caused by the loss of function of the maternal copy of the UBE3A gene. Previous studies reported an increase in α1-Na/K-ATPase (α1-NaKA) expression in the AS hippocampus at the age of 2 weeks as the initial and isolated molecular alteration. This increase was further implied upon actuating much of the hippocampal-related deficits in an AS mouse model, although the underlying mechanism was never investigated. Here, we showed that enhanced α1-NaKA expression resulted in increased pump activity that reduced activity-dependent dendritic Ca2+ dynamics in the AS hippocampus, as well as selective inhibition of α1-NaKA by marinobufagenin (MBG) to normalize these aberrant Ca2+ dynamics. In addition, we demonstrated that selective α1-NaKA inhibition corrected impaired hippocampal synaptic plasticity and hippocampal-dependent cognitive deficits. Furthermore, we showed that the isolated increase in hippocampal α1-NaKA expression in AS mice at 2 weeks of age was accompanied by an unexpected enhancement in excitability. Altogether, our study implicates the modification of Ca2+ dynamics as one of the major underlying mechanisms by which enhanced α1-NaKA expression induces deleterious effects in the hippocampus of AS model mice. Finally, we propose a therapeutic approach for AS and possibly other neurodevelopmental disorders that entail aberrant NaKA expression or abnormal Ca2+ dynamics." @default.
• W2969156715 created "2019-08-22" @default.
• W2969156715 creator A5015556456 @default.
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• W2969156715 creator A5060576389 @default.
• W2969156715 date "2019-11-01" @default.
• W2969156715 modified "2023-09-26" @default.
• W2969156715 title "α1-Na/K-ATPase inhibition rescues aberrant dendritic calcium dynamics and memory deficits in the hippocampus of an Angelman syndrome mouse model" @default.
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• W2969156715 doi "https://doi.org/10.1016/j.pneurobio.2019.101676" @default.
• W2969156715 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31401139" @default.
• W2969156715 hasPublicationYear "2019" @default.
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