STREPCO

"Stress, Prefrontal function and Cognition: Role of the Glucocorticoid Receptor"

 Coordinatore CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE 

 Organization address address: Rue Michel -Ange 3
city: PARIS
postcode: 75794

contact info
Titolo: Mr.
Nome: Louis
Cognome: Avigdor
Email: send email
Telefono: 33142349417

 Nazionalità Coordinatore France [FR]
 Totale costo 202˙405 €
 EC contributo 202˙405 €
 Programma FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call FP7-PEOPLE-2013-IIF
 Funding Scheme MC-IIF
 Anno di inizio 2014
 Periodo (anno-mese-giorno) 2014-09-01   -   2016-08-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE

 Organization address address: Rue Michel -Ange 3
city: PARIS
postcode: 75794

contact info
Titolo: Mr.
Nome: Louis
Cognome: Avigdor
Email: send email
Telefono: 33142349417

FR (PARIS) coordinator 202˙405.80

Mappa

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 Word cloud

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microcircuit    pfc    symptoms    alter    mechanisms    brain    action    gcs    cognitive    interneurons    induced    stress    behavioral    gr    deficits    suggested    psychiatric    pyramidal    receptor    disorders    cognition    cell    prefrontal   

 Obiettivo del progetto (Objective)

'Cognitive deficits are hallmark features of a variety of psychiatric diseases. While body of evidences pointed to the prefrontal cortex (PFC) as a key structure for cognition, recent studies further suggested that abnormalities in the interaction between inhibitory interneurons and glutamatergic pyramidal cells within PFC microcircuit could be involved in the pathogenesis of cognitive deficits in psychiatric disorders. Thus, intensive effort has been made to understand the mechanisms underlying PFC microcircuit dysfunction and the ensuing cognitive impairment. Stress-induced release of glucocorticoids (GCs) has been associated with cognitive symptoms in multiple mental disorders. GCs modulate behavioral responses to stress via their binding to the glucocorticoid receptor (GR), a nuclear receptor expressed in heterogeneous cell populations throughout the brain. Although it has been suggested that GCs could alter cognition through their action within the PFC, it is still unknown whether and how the GCs via their action on distinct cell types within the PFC can alter cognition, prefrontal microcircuit function and larger brain circuits. Only a genetic approach offering spatial resolution and cell-type specificity can precisely address these issues. Given their key role in cognition and their potential involvement in the pathophysiology of psychiatric disorders, I propose to manipulate GR expression within PFC pyramidal neurons and Parvalbumin-expressing interneurons. Using a battery of PFC-dependant cognitive tasks, I will study the behavioral consequences of these manipulations. Finally, combining whole cell patch-clamp and in vivo multisite recordings in behaving mice, I will assess the functional impact of GR gene manipulation on PFC microcircuit and hippocampo-frontal network during working memory. This study should shed light on mechanisms involved in stress-induced cognitive deficit and potentially lead to the finding of new treatment against cognitive symptoms.'

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