BEGIN:VCALENDAR VERSION:2.0 PRODID:-//Memento EPFL// BEGIN:VEVENT SUMMARY:Neural Circuits & Behavior Process Report // Laia Morato - Stress- induced alterations of eNAMPT impair NAD+/SIRT1 pathway in the nucleus acc umbens and reduce sociability DTSTART:20190307T093000 DTEND:20190307T103000 DTSTAMP:20260407T042057Z UID:c25055c6d2ab6a6c2e9986845222eef4d1c234f62112b76690add33b CATEGORIES:Conferences - Seminars DESCRIPTION:Laia Morato \, Prof. Sandi's lab\n\nEarly-life exposure to str essful experiences has been described as a predisposing factor to develop alterations both in metabolism and behavior. Here\, we show that exposure to a paradigm of unpredictable stress during the peripubertal period reduc es sociability in mice together with alterations in peripheral metabolism\ , such as increased percentage of fat mass. Remarkably\, the protein level s of NAMPT in the adipose tissue of stressed mice are decreased and the bl ood levels of the cytokine eNAMPT -the extracellular form of the enzyme- p redict the behavioral deficits displayed later in life. Aiming at understa nding whereby eNAMPT differences can cause alterations in the brain\, we a nalyzed NAD+ levels\, expression of mitochondrial genes and neuronal excit ability in the nucleus accumbens (NAc)\, a key brain region for the stress response. We observed that the NAc of stressed mice exhibits an impairmen t in the NAD+/SIRT1 pathway together with reduced neuronal excitability. S ystemic treatment with the NAD+ booster nicotinamide mononucleotide (NMN) or adipose-specific overexpression of Nampt prevents sociability and neuro nal excitability deficits in the NAc. Moreover\, genetic and pharmacologic al modulation of SIRT1 expression in the NAc rescues sociability deficits. These findings strengthen the idea of eNAMPT as a mediator of fat-brain c ommunication and pave the way for the use of NAD+ boosters to treat stress -related disorders such as depression.\n  LOCATION:SV 1717 https://plan.epfl.ch/?room==SV%201717 STATUS:CONFIRMED END:VEVENT END:VCALENDAR