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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.

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

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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