DEFINE SIGNED
DEciphering mechanisms of presynaptic reFINEment
Total Cost €
0EC-Contrib. €
0Partnership
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Explore the words cloud of the DEFINE project. It provides you a very rough idea of what is the project "DEFINE" about.
Project "DEFINE" data sheet
The following table provides information about the project.
| Coordinator |
AGENCIA ESTATAL CONSEJO SUPERIOR DEINVESTIGACIONES CIENTIFICAS
Organization address contact info |
| Coordinator Country | Spain [ES] |
| Total cost | 172˙932 € |
| EC max contribution | 172˙932 € (100%) |
| Programme |
1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility) |
| Code Call | H2020-MSCA-IF-2019 |
| Funding Scheme | MSCA-IF-EF-RI |
| Starting year | 2020 |
| Duration (year-month-day) | from 2020-10-01 to 2022-09-30 |
Partnership
Take a look of project's partnership.
| # | ||||
|---|---|---|---|---|
| 1 | AGENCIA ESTATAL CONSEJO SUPERIOR DEINVESTIGACIONES CIENTIFICAS | ES (MADRID) | coordinator | 172˙932.00 |
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Project objective
The postdoctoral project aims to investigate the mechanisms underlying sensory experience driven synaptic and circuit refinement that occurs during critical periods of brain development. Presynaptic and postsynaptic refinement involving loss and strengthening of synaptic contacts are known to occur but how these processes are coordinated and remains obscure. Failure to appropriately regulate this refinement underlies some common neurological disorders including autism and schizophrenia. The non-canonical NMDA-receptor subunit GluN3A presents a likely key factor in the timely remodelling of these circuits. This project will interrogate the completely unknown roles GluN3A plays in presynaptic postnatal refinement processes. The cellular location and trans-synaptic coordination that may define these events mediated by GluN3A will be carefully dissected through analysis of interhemispheric callosal projection axons using targeted delivery of transgenic reagents by in utero electroporation in the mouse brain. Chemogenetic and sensory deprivation approaches will provide exquisite control over activity and experience dependent roles within this refinement over critical windows of development. Revealing of cellular and molecular mechanisms that GluN3A functions through in presynaptic and axonal development will be guided by unbiased RNAseq data and explored via the latest cellular and transgenic tools. Follow up experiments assessing functional connectivity, in collaboration with colleagues at the hosting institute, will help understand the impacts on circuit function and synaptic communication arising from morphological changes of GluN3A perturbation and thus understand how healthy circuits and behaviour develop. A clearer knowledge of the molecular regulation of this synaptic restructuring from the perspective of the entire circuit and its modulation by experience during development may allow for improved therapeutic intervention in neurodevelopmental disorders.
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