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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.

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

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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