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NMDARETT

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

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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.

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

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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