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- W1790544538 endingPage "51" @default.
- W1790544538 startingPage "41" @default.
- W1790544538 abstract "Nicotinamide adenine dinucleotide (NAD(+)) is an essential coenzyme/cosubstrate for many biological processes in cellular metabolism. The rate-limiting step in the major pathway of mammalian NAD(+) biosynthesis is mediated by nicotinamide phosphoribosyltransferase (Nampt). Previously, we showed that mice lacking Nampt in forebrain excitatory neurons (CamKIIαNampt(-/-) mice) exhibited hyperactivity, impaired learning and memory, and reduced anxiety-like behaviors. However, it remained unclear if these functional effects were accompanied by synaptic changes. Here, we show that CamKIIαNampt(-/-) mice have impaired induction of long-term depression (LTD) in the Schaffer collateral pathway, but normal induction of long-term potentiation (LTP), at postnatal day 30. Pharmacological assessments demonstrated that CamKIIαNampt(-/-) mice also display dysfunction of synaptic GluN2B (NR2B)-containing N-methyl-d-aspartate receptors (NMDARs) prior to changes in NMDAR subunit expression. These results support a novel, important role for Nampt-mediated NAD(+) biosynthesis in LTD and in the function of GluN2B-containing NMDARs." @default.
- W1790544538 created "2016-06-24" @default.
- W1790544538 creator A5013140480 @default.
- W1790544538 creator A5067324638 @default.
- W1790544538 creator A5081481500 @default.
- W1790544538 creator A5082716238 @default.
- W1790544538 date "2015-10-01" @default.
- W1790544538 modified "2023-10-18" @default.
- W1790544538 title "Nampt is required for long-term depression and the function of GluN2B subunit-containing NMDA receptors" @default.
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