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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.

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

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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