Opendata, web and dolomites

Somnostat SIGNED

The Homeostatic Regulation and Biological Function of Sleep

Total Cost €

0

EC-Contrib. €

0

Partnership

0

Views

0

 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.

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

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.

Are you the coordinator (or a participant) of this project? Plaese send me more information about the "SOMNOSTAT" project.

For instance: the website url (it has not provided by EU-opendata yet), the logo, a more detailed description of the project (in plain text as a rtf file or a word file), some pictures (as picture files, not embedded into any word file), twitter account, linkedin page, etc.

Send me an  email (fabio@fabiodisconzi.com) and I put them in your project's page as son as possible.

Thanks. And then put a link of this page into your project's website.

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

More projects from the same programme (H2020-EU.1.1.)

CHIPTRANSFORM (2018)

On-chip optical communication with transformation optics

Read More  

CUSTOMER (2019)

Customizable Embedded Real-Time Systems: Challenges and Key Techniques

Read More  

AncientAdhesives (2019)

Ancient Adhesives - A window on prehistoric technological complexity

Read More