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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.

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

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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