FUELLINGSYNAPSES

Regulation of neuronal connectivity and plasticity by activity-dependent mitochondrial trafficking to synapses

 Coordinatore UNIVERSITY COLLEGE LONDON 

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 Nazionalità Coordinatore United Kingdom [UK]
 Totale costo 1˙997˙567 €
 EC contributo 1˙997˙567 €
 Programma FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call ERC-2011-StG_20101109
 Funding Scheme ERC-SG
 Anno di inizio 2012
 Periodo (anno-mese-giorno) 2012-02-01   -   2017-01-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITY COLLEGE LONDON

 Organization address address: GOWER STREET
city: LONDON
postcode: WC1E 6BT

contact info
Titolo: Dr.
Nome: Josef
Cognome: Kittler
Email: send email
Telefono: +44 20 7679 3218
Fax: +44 20 7679 7298

UK (LONDON) hostInstitution 1˙997˙567.00
2    UNIVERSITY COLLEGE LONDON

 Organization address address: GOWER STREET
city: LONDON
postcode: WC1E 6BT

contact info
Titolo: Mr.
Nome: Giles
Cognome: Machell
Email: send email
Telefono: +44 020 3108 3020
Fax: +44 020 7813 2849

UK (LONDON) hostInstitution 1˙997˙567.00

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

molecular    connectivity    mitochondria    mitochondrial    correct    plasticity    trafficking    neuronal    dependent    miro    mechanisms    synapses    calcium    regulating    neurons    function    determine   

 Obiettivo del progetto (Objective)

'Regulated trafficking of mitochondria is essential for providing ATP at the correct spatial location to power neural computation, and for providing calcium buffering at sites of calcium entry or release. In neurons, the concentration of mitochondria in specific regions such as growth cones and synapses is important for correct neuronal function and development. Moreover mutations in proteins regulating mitochondrial trafficking compromise neuronal development and the formation, function and plasticity of synapses, and defective mitochondrial trafficking is increasingly implicated in neurological diseases. Understanding the molecular mechanisms that allow neurons to tailor the distribution of mitochondria to changes in neuronal activity therefore has important implications for our understanding of neuronal function and communication. This proposal will study the mechanisms that control the trafficking of the energy providing mitochondria within neurons, and how this relates to neuronal connectivity and plasticity. Using imaging, electrophysiological, molecular and cell biological techniques, combined with viral transduction and mouse transgenic approaches we will determine the molecular mechanisms underlying the activity-dependent subcellular positioning of mitochondria in neurons. We will examine how the mitochondrial Ca2-sensing GTPases Miro1 and Miro2 act to regulate mitochondrial movement, distribution and function and how this contributes to neuronal development, synaptogenesis and synaptic plasticity. A key goal will be to determine if different roles exist for constitutive versus activity-dependent control of mitochondrial transport by Miro1 and Miro2 in these processes. These studies will significantly advance our understanding of the molecular mechanisms that control mitochondrial localisation in neurons and the role that activity-dependent mitochondrial trafficking plays in regulating neuronal development, morphogenesis, connectivity and function.'

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