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Somnostat SIGNED

The Homeostatic Regulation and Biological Function of Sleep

Total Cost €

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EC-Contrib. €

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Partnership

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 Somnostat project word cloud

Explore the words cloud of the Somnostat project. It provides you a very rough idea of what is the project "Somnostat" about.

aging    signals    mammalian    cellular    seek    oxidative    responds    autonomous    broad    rho    leak    vice    first    shaker    redox    data    persistently    endocytosis    versa    nicotinamide    mitochondrial    subunit    encoded    dozen    unknown    biological    exist    sleep    disease    central    electrically    independently    mechanistic    understand    vital    dorsal    inducing    body    membrane    preliminary    strengthen    revealing    switching    bound    channel    voltage    electron    universal    lifespan    synaptic    gtpase    cofactor    beta    drosophila    implicated    insights    drive    excitability    modulated    responsible    intrinsic    hypothalamus    shaped    pressure    silent    monitor    transport    stress    consequence    respiration    biophysics    chemistry    extraction    validity    metabolism    neurons    connection    disruptions    dfb    gated    waking    perturbing    regulated    electrical    energy    prerequisite    rising    antagonistically    mechanisms    brain    fluctuates    molecular    activates    relay    gained    function    question    conductances    gtpases    sandman    parallels    transducers    machinery    potassium    plasma    hyperkinetic    showed    cell    nature    clear    fan    active    point   

Project "Somnostat" data sheet

The following table provides information about the project.

Coordinator
THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD 

Organization address
address: WELLINGTON SQUARE UNIVERSITY OFFICES
city: OXFORD
postcode: OX1 2JD
website: www.ox.ac.uk

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country United Kingdom [UK]
 Total cost 2˙374˙999 €
 EC max contribution 2˙374˙999 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2018-ADG
 Funding Scheme ERC-ADG
 Starting year 2019
 Duration (year-month-day) from 2019-10-01   to  2024-09-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE CHANCELLOR, MASTERS AND SCHOLARS OF THE UNIVERSITY OF OXFORD UK (OXFORD) coordinator 2˙374˙999.00

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 Project objective

Sleep is vital and universal, but its biological function remains unknown. This project will seek to understand why we need to sleep by studying how the brain responds to sleep loss. My previous work in Drosophila showed that rising sleep pressure activates two dozen sleep-inducing neurons in the dorsal fan-shaped body (dFB) of the central complex. Sleep need is encoded in the electrical excitability of these neurons, which fluctuates because two potassium conductances, voltage-gated Shaker and the leak channel Sandman, are modulated antagonistically. As a consequence, dFB neurons are electrically silent during waking and persistently active during sleep. The key open question addressed in this project is the nature of the molecular changes that drive dFB neurons into the electrically active state. My preliminary data point to two dFB-intrinsic transducers of sleep pressure. First, the Shaker β subunit Hyperkinetic responds via a bound nicotinamide cofactor to oxidative by-products of mitochondrial electron transport, revealing a potential connection between energy metabolism, oxidative stress, and sleep, three processes implicated independently in lifespan, aging, and disease. To strengthen this connection, we will monitor sleep and the biophysics of dFB neurons after perturbing mitochondrial respiration or cellular redox chemistry and vice versa. Second, Rho GTPases relay currently unknown signals to the machinery responsible for the regulated endocytosis of Sandman, whose extraction from the plasma membrane is a prerequisite for switching the sleep-promoting activity of dFB neurons on. To identify these signals, we will investigate cell-autonomous, synaptic, and non-synaptic mechanisms of GTPase control. Because clear parallels exist between dFB neurons and sleep-active neurons in the mammalian hypothalamus, mechanistic insights that can currently be gained only in Drosophila are expected to have broad validity for understanding sleep and its disruptions.

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The information about "SOMNOSTAT" are provided by the European Opendata Portal: CORDIS opendata.

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