HOMEOSTASIS_IN_VIVO

Mechanisms of homeostatic plasticity in the intact mouse visual cortex

 Coordinatore UNIVERSITY COLLEGE LONDON 

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 Nazionalità Coordinatore United Kingdom [UK]
 Totale costo 1˙494˙473 €
 EC contributo 1˙494˙473 €
 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-2012-StG_20111109
 Funding Scheme ERC-SG
 Anno di inizio 2013
 Periodo (anno-mese-giorno) 2013-01-01   -   2017-12-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    KING'S COLLEGE LONDON

 Organization address address: Strand
city: LONDON
postcode: WC2R 2LS

contact info
Titolo: Dr.
Nome: Paul
Cognome: Labbett
Email: send email
Telefono: +44 2078486136

UK (LONDON) beneficiary 115˙677.70
2    UNIVERSITY COLLEGE LONDON

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

contact info
Titolo: Dr.
Nome: Tara
Cognome: Keck Lesica
Email: send email
Telefono: +44 2078486514
Fax: +44 2076797298

UK (LONDON) hostInstitution 1˙378˙796.23
3    UNIVERSITY COLLEGE LONDON

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

contact info
Titolo: Mr.
Nome: Daniele
Cognome: Giannone
Email: send email
Telefono: +44 0 20 3108 9373

UK (LONDON) hostInstitution 1˙378˙796.23

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 Word cloud

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sensory    cortex    cell    visual    intact    homeostatic    hebbian    us    mechanisms    degree    mouse    deprivation    plasticity    function    questions    paradigm    cells    synaptic   

 Obiettivo del progetto (Objective)

'Changes in input lead to changes of synaptic circuits in the brain via a combination of synapse specific Hebbian plasticity and cell-wide homeostatic plasticity. While Hebbian plasticity has been well studied, there are still a number of outstanding fundamental questions related to homeostatic plasticity. We have previously developed a paradigm that allows us to monitor changes to multiple homeostatic mechanisms in the intact mouse visual cortex following sensory deprivation. We will use this paradigm together with chronic two-photon imaging of synaptic structures and function, via genetically encoded calcium indicators in awake behaving animals. These techniques allow us to measure the structure and function from the same synapses and cells over a period of weeks to months, both before and after sensory deprivation. In the work proposed here, we will investigate two basic principles of homeostatic plasticity: 1) the spatial scale at which homeostatic mechanisms occur – is it at the level of individual dendrites or are all changes implemented cell-wide? and 2) the relationship between homeostatic plasticity and the degree of changing activity levels in cells and networks of cells – is the degree of resulting homeostatic plasticity dependent on the level of deprivation? If so, can changes in dendritic activity, cellular activity or network activity drive these changes? We will investigate these questions for both excitatory and inhibitory neurons in the intact mouse visual cortex for two forms of homeostatic plasticity – synaptic scaling and the balance between excitation and inhibition.'

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