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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.

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

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

Map

 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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