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CLAUSTROFUNCT SIGNED

Claustrum function in cortical processing and putative claustral dysfunction in schizophrenia

Total Cost €

0

EC-Contrib. €

0

Partnership

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 CLAUSTROFUNCT project word cloud

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

causal    delusions    dysfunction    mouse    reports    prefrontal    uniquely    expressing    underlying    hallucinations    light    function    causes    suggesting    suggest       traits    pfc    kappa    enigmatic    receptor    regulating    levels    patients    cortices    cla    interconnected    summary    neocortex    disease    behavioral    centers    incidence    risk    circuits    circuit    works    combination    hallucinogenic    hypothesize    impaired    unknown    transient    functions    mechanisms    lesions    search    worldwide    led    positioned    found    associative    link    claustrum    symptoms    selectively    concomitantly    genes    evidences    deficits    schizophrenia    medical    permanent    subcortical    communication    expressed    reciprocally    cortex    opioid    exact    executive    pathology    altered    malfunction    shed    expression    chronic    potentially    potent    played    peculiar    highest    cortical    normal    mental    nature    network    drug    brain    establishing    structure    influence    cognitive    salvinorin   

Project "CLAUSTROFUNCT" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITE DE GENEVE 

Organization address
address: RUE DU GENERAL DUFOUR 24
city: GENEVE
postcode: 1211
website: www.unige.ch

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 Switzerland [CH]
 Total cost 5˙000˙000 €
 EC max contribution 5˙000˙000 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2019-SyG
 Funding Scheme ERC-SyG
 Starting year 2020
 Duration (year-month-day) from 2020-04-01   to  2026-03-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITE DE GENEVE CH (GENEVE) coordinator 5˙000˙000.00

Map

 Project objective

Schizophrenia is a chronic mental disease having an incidence of 1% worldwide. Its symptoms are numerous and range from hallucinations to altered executive functions. Although the exact causes of schizophrenia are unknown, several works suggest that impaired communication between higher cortical centers may be important for the expression of the disease. Establishing a causal link between circuit function (and/or dysfunction) and particular behavioral traits relevant to schizophrenia may shed new light on the mechanisms underlying the pathology. Dysfunction of the prefrontal cortex (PFC) may contribute to cognitive deficits relevant to schizophrenia. In a search for circuits potentially regulating the PFC, we identified an enigmatic and not well-studied network, the claustrum (CLA). This subcortical structure of unknown function is supposed to be highly reciprocally interconnected with the neocortex, especially associative cortices involved in behavioral traits relevant to schizophrenia. It is thus uniquely positioned to influence cortical communication. The CLA is also peculiar because it represents the brain structure expressing the highest levels of kappa opioid receptor, the receptor of the most potent hallucinogenic drug found in nature, salvinorin A, suggesting a potential role played by the CLA in hallucinations. This link is further supported by medical reports in which patients having transient or permanent lesions in the claustrum develop hallucinations and delusions concomitantly. Finally, many risk factors genes associated to schizophrenia are strongly and often selectively expressed in the mouse claustrum. In summary, this combination of evidences led us to hypothesize that the claustrum may represent a circuit whose malfunction is relevant to the expression of schizophrenia. Our proposal will test the role of the claustrum in the normal brain and test whether its dysfunction may contribute to schizophrenia symptoms.

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