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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.

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

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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