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NMDARETT

Cell-type Specific Mechanisms and Functional Consequences of Altered NMDA Receptor Development and Mecp2 Deficiency on Developing Cortical Circuits

Total Cost €

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EC-Contrib. €

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Partnership

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 NMDARETT project word cloud

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

sequencing    synapses    controls    mea    hypothesize    autism    deficient    expression    wellcome    defects    disruption    rett    career    leads    rescued    genetic    cambridge    genomic    network    disorders    imbalance    therapies    altered    combine    causes    trust    single    manipulation    calcium    neurologist    prepare    differentially    imaging    pv    premature    regulation    receptor    excitatory    functional    recording    cells    mice    cultures    cutting    me    nmda    training    mecp2    deficiency    rna    circuits    receptors    positive    full    accelerating    syndrome    techniques    cortical    of    electrode    inhibition    mechanisms    nmdar    underlying    independent    showed    photon    recordings    synaptic    maturation    slowing    types    edge    sanger    alters    multiple    parvalbumin    circuit    interneurons    neurons    university    function    neuroscientist    inhibitory    dysfunction    neurodevelopmental    excitation    pyramidal    array    idea    elucidate    cell   

Project "NMDARETT" data sheet

The following table provides information about the project.

Coordinator
THE CHANCELLOR MASTERS AND SCHOLARSOF THE UNIVERSITY OF CAMBRIDGE 

Organization address
address: TRINITY LANE THE OLD SCHOOLS
city: CAMBRIDGE
postcode: CB2 1TN
website: www.cam.ac.uk

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 United Kingdom [UK]
 Project website https://www.pdn.cam.ac.uk/directory/susanna-mierau
 Total cost 195˙454 €
 EC max contribution 195˙454 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2015
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2016
 Duration (year-month-day) from 2016-04-01   to  2018-08-02

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE CHANCELLOR MASTERS AND SCHOLARSOF THE UNIVERSITY OF CAMBRIDGE UK (CAMBRIDGE) coordinator 195˙454.00

Map

 Project objective

NMDA receptor (NMDAR) dysfunction has been identified in multiple genetic causes of autism and related neurodevelopmental disorders. I recently showed that loss of Mecp2, the cause of Rett syndrome and some cases of autism, differentially affects NMDAR development at cortical synapses on specific cell-types: slowing down the development in excitatory pyramidal neurons and accelerating the maturation in parvalbumin-positive (PV) inhibitory interneurons. Genetic manipulation of NMDAR expression in Mecp2-deficient mice rescued both cortical function and the premature NMDAR maturation in PV cells. Based on these findings, I hypothesize that this cell-type specific disruption of NMDAR development leads to an imbalance in excitation and inhibition in the developing cortical circuits. To test this idea, I will combine single cell genomic and cell-type specific recording techniques to elucidate how Mecp2 controls the development of synaptic receptors and the impact on network function. In Aim 1, I will use cutting-edge techniques for single-cell RNA sequencing and synaptic recordings of NMDAR maturation in cortical cultures to identify novel cell-type specific mechanisms underlying NMDAR development and the regulation by Mecp2. In Aim 2, I will investigate the functional effects of Mecp2 deficiency and altered NMDAR maturation on the development of cortical network activity using two-photon calcium imaging and multi-electrode array (MEA) recordings. As a neuroscientist and neurologist, this training will prepare me for an independent research career addressing the circuit-based defects underlying Rett syndrome and autism. I have the full support of the University of Cambridge and Wellcome Trust Sanger Institute for the proposed research and my career development. This study will improve our understanding of how loss of Mecp2 alters cortical circuits and has the potential to identify novel cell-type specific targets for developing new therapies for Rett syndrome.

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