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SCAMPICITY

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Cerrado

cAMP dependend plasticity of striatal projection neurons in health and disease

The project aims to reveal the so far unknown role of cAMP in structural and synaptic plasticity of striatal spiny projection neurons (SPNs) in health and disease. Striatal SPNs divide into two subgroups: the dSPNs and iSPNs. Whil... ver más

31/03/2021

UKE

175K€

Presupuesto del proyecto: 175K€

Líder del proyecto

UNIVERSITAETSKLINIKUM HAMBURGEPPENDORF No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Fecha límite participación Sin fecha límite de participación.

Financiación concedida El organismo H2020 notifico la concesión del proyecto el día 2021-03-31

MSCA-IF-2018: Individual Fellowships

I+D

Cerrada hace 6 años

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

1 Participantes

UKE

174.81K€ | Lider

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Duración del proyecto: 24 meses Fecha Inicio: 2019-03-21
Fecha Fin: 2021-03-31

Líder del proyecto

UNIVERSITAETSKLINIKUM HAMBURGEPPENDORF No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 175K€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto The project aims to reveal the so far unknown role of cAMP in structural and synaptic plasticity of striatal spiny projection neurons (SPNs) in health and disease. Striatal SPNs divide into two subgroups: the dSPNs and iSPNs. While dSPNs preferentially express the D1 dopamine (DA) receptor, iSPNs express the D2 receptor. Both are coupled to the cAMP second messenger cascade, however the D1-receptor activates and the D2-receptor inhibits it. DA has therefore opposite effects on the two SPN groups, both mediated by cAMP. Parkinson’s disease (PD) is the second most common neurodegenerative disorder. It is characterized by typical motor symptoms caused by the death of DA neurons and the subsequent lack of DA in the striatum. A long-standing but untested notion in the field is that loss of DA leads to aberrant cAMP levels and signaling in SPNs. The project will look at the role of cAMP in SPN synaptic and structural plasticity. We will use novel optogenetic tools that allow cell-type specific activation of cAMP, with high spatiotemporal resolution. Focusing on corticostriatal synaptic transmission, we want to ask if transient activation of cAMP alone is sufficient to induce plasticity (e.g. strengthening or weakening) of this synapse. Secondly, we will use known plasticity protocols and test if precise activation of cAMP can interrupted or potentiated them. Unpublished data suggest that in vivo drug treatments that presumably elevate cAMP in SPNs induce structural plasticity, i.e. loss of dendritic spines. Following this we will unravel if cell-type specific activation of cAMP is sufficient to induce structural changes and how this relates to synaptic plasticity. Lastly, we will test the long-standing notion that cAMP levels and the responsiveness of the cascade are altered in an animal model of PD. This project will advance our understanding of how SPNs work by unraveling cAMP’s role in plasticity, and potentially inform future strategies to combat PD.

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