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StressPFCog SIGNED

Mechanisms of stress-induced cognitive deficits : Role of the glucocorticoid receptor and its partners in the regulation of PFC function.

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 StressPFCog project word cloud

Explore the words cloud of the StressPFCog project. It provides you a very rough idea of what is the project "StressPFCog" about.

interplay    ultimately    disorders    abnormal    exposure    memory    circuit    mediated    locus    molecular    hormone    flexibility    physiology    remodeler    expressing    manipulations    conditional    exert    networks    glucocorticoid    behavioural    correlates    thereby    recordings    cortex    either    binding    behaving    cognitive    illness    schizophrenia    transcription    transfer    electrophysiology    basal    poorly    depression    neurons    multisite    midbrain    modify    stress    chromatin    function    combining    cellular    viral    gene    linked    chronic    gr    executive    dysfunction    pfc    receptor    discrete    impairment    psychiatric    species    action    pyramidal    deficits    modulate    cell    cognition    decline    co    genes    expressed    variety    inactivate    mechanisms    mutagenesis    gcs    expression    circuits    hippocampus    brain    prefrontal    interneurons    examine    vulnerable    underpinnings    impairments    mice    populations    mental    risk    brg1    environmental    detrimental    reported    parvalbumin    levels    physiological    neuronal   

Project "StressPFCog" data sheet

The following table provides information about the project.

Coordinator
CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE CNRS 

Organization address
address: RUE MICHEL ANGE 3
city: PARIS
postcode: 75794
website: www.cnrs.fr

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 France [FR]
 Total cost 173˙076 €
 EC max contribution 173˙076 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2016
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2018
 Duration (year-month-day) from 2018-01-04   to  2020-01-03

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE CNRS FR (PARIS) coordinator 173˙076.00

Map

 Project objective

The prefrontal cortex (PFC) is a locus for higher-order cognition and executive control across species. In most mental disorders such as depression or schizophrenia, dysfunction in PFC and its related neuronal networks has been associated with a variety of cognitive impairments. Chronic stress exposure and abnormal levels of glucocorticoid stress hormone (GCs) is a key environmental risk factor for psychiatric illness. The PFC is highly vulnerable to stress exposure and many studies have reported detrimental effects of chronic stress exposure and/or high GCs levels on cognition, however the physiological underpinnings remain poorly understood. GCs exert their action in part by binding the glucocorticoid receptor (GR), a transcription factor expressed in every cell type. Through a complex interplay with co-factors, GR can modulate the expression of a large set of genes and thereby modify brain circuit physiology ultimately leading to behavioural changes. In this project, I propose to investigate the molecular and cellular mechanisms through which stress-exposure can modify the activity of PFC and its related networks and lead to cognitive impairment. Combining viral-mediated gene transfer and conditional mutagenesis in mice, I propose to inactivate GR either within the whole PFC or in discrete PFC cell populations namely the pyramidal neurons or the parvalbumin-expressing interneurons. I will study the impact of these manipulations on cognitive function including working memory and behavioural flexibility under basal conditions or after chronic stress exposure. The physiological correlates of cognitive deficits will be investigated using multisite electrophysiology recordings in behaving mice with a specific focus on PFC-hippocampus-midbrain circuits. Finally, I propose to examine the PFC-specific role of an important GR binding partner called BRG1, a chromatin remodeler recently linked to cognitive decline in several psychiatric conditions.

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

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