CELLSYNCIRCUITS

CELLULAR AND SYNAPTIC DISSECTION OF THE NEURONAL CIRCUITS OF SOCIAL AND AUTISTIC BEHAVIOR

 Coordinatore CENTRO DE NEUROCIENCIAS E BIOLOGIACELULAR ASSOCIACAO 

 Organization address address: UNIVERSIDADE DE COIMBRA .
city: COIMBRA
postcode: 3004 517

contact info
Titolo: Prof.
Nome: Ana Luisa
Cognome: Carvalho
Email: send email
Telefono: +351 239820190

 Nazionalità Coordinatore Portugal [PT]
 Totale costo 100˙000 €
 EC contributo 100˙000 €
 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-CIG
 Funding Scheme MC-CIG
 Anno di inizio 2013
 Periodo (anno-mese-giorno) 2013-08-01   -   2017-07-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    CENTRO DE NEUROCIENCIAS E BIOLOGIACELULAR ASSOCIACAO

 Organization address address: UNIVERSIDADE DE COIMBRA .
city: COIMBRA
postcode: 3004 517

contact info
Titolo: Prof.
Nome: Ana Luisa
Cognome: Carvalho
Email: send email
Telefono: +351 239820190

PT (COIMBRA) coordinator 100˙000.00

Mappa


 Word cloud

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disorders    social    genetic    circuits    behavioral    dysfunction    affiliative    synaptic    behaviors    cellular    schizophrenia    autism   

 Obiettivo del progetto (Objective)

'Synapses are the cellular specializations responsible for transducing information between neurons. Synaptic dysfunction is thought to underlie disorders such as schizophrenia, autism and mental retardation. Currently, a major challenge for modern neuroscience is to understand how synaptic computations give rise to behavioural and cognitive programs and identify how these same circuits are affected in neuropsychiatric disorders. At present, a multitude of factors both genetic and environmental are recognized to impact on the etiology of autism spectrum disorders (ASDs) and schizophrenia. Nevertheless, and while these disorders diverge on several factors such as, typical age of onset, language skills and other clinical presentations; convergence is observed in several behavioral phenotypes and in genetic mutations common to both disorders. Indeed, a prominent feature in the symptomatology of both conditions is a dysfunction in social behaviors. However, the synaptic circuits and pathways that regulate the expression of affiliative social behaviors remain largely unknown. To begin shedding light on these complex behaviors and neural circuits, we are dissecting the cellular and synaptic maps of ethologically relevant affiliative social behaviors using a multidisciplinary approach combining genetic and optogenetic tools. We are also modulating neuronal synaptic circuits in genetic and behavioral mouse models of autism and schizophrenia. Our strategy will unravel the primitive brain centers controlling social behavior in mammals and address how disruption in sociability may lead to common dysfunctions that may be transversal to several human disorders.'

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