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SPICED

Financiado

Cerrado

Spine plasticity in changing environment and diseases

Given the persistence of stress-related disorders, it is critical to identify the circuits, cells and mechanisms that fail to recover from stressor exposure. The stress hormone glucocorticoid causes reversible remodeling of brain... ver más

28/02/2018

CNRS

100K€

Presupuesto del proyecto: 100K€

Líder del proyecto

CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE... No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Fecha límite participación Sin fecha límite de participación.

Ver 2 Participantes

Financiación concedida El organismo FP7 notifico la concesión del proyecto el día 2018-02-28 No tenemos la información de la convocatoria

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Información adicional privada

No hay información privada compartida para este proyecto. Habla con el coordinador.

2 Participantes

CNRS

0.00€ | Lider

INSERM

N.D. | Participante

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Líder del proyecto

CENTRE NATIONAL DE LA RECHERCHE SCIENTIFIQUE... No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 100K€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto Given the persistence of stress-related disorders, it is critical to identify the circuits, cells and mechanisms that fail to recover from stressor exposure. The stress hormone glucocorticoid causes reversible remodeling of brain circuits involved in cognitive, executive and hedonic behaviors. While small amounts of glucocorticoids support cognition and spine synapse turnover, excess stimulation by glucocorticoids predisposes to stress disorders via the loss of dendritic spines. To date, however, because of the paucity of knowledge of underlying mechanisms, deleterious effects of glucocorticoids are not prevented following extreme stress. My model predicts a fine balance exists between the spine formation and spine elimination needed for behavioral adaptation to stress. Which spines survive, which spines are eliminated may encode the structural basis of learning adaptive behavior. There is hope that promoting dendritic spine turnover facilitates recovery from stressful experience, and paves the road for the discovery of better drug treatments for disorders featuring disrupted glucocorticoid circadian rhythms. One hypothesis to account for the onset and severity of these disorders is that glucocorticoid actions diverge as a function of brain-derived neurotrophic factor (BDNF) signaling. Using mouse genetics, behavior, in vivo imaging and transcriptomic, the SPICED project aims at charactering a novel neurotrophic-sensing mechanism of glucocorticoid actions on spine turnover in changing environment. The SPICED project capitalizes on robust preliminary data arguing that BDNF signaling employs the phosphorylated glucocorticoid receptor (GR) as transcription factor to produce a unique gene expression signature. Should BDNF-induced GR phosphorylation become impaired, appropriate turnover of dendritic spines to durable stress or excess glucocorticoids may be inhibited thus setting the stage for neural network wiring defects and development of neuropsychiatric disorders.

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