ESR1
    ESR2
    ESR3
    ESR4
    ESR5
    ESR6
    ESR7
    ESR8
    ESR9
    ESR10
    ESR11
    ER1
    ER2
    ER3


Project Co-ordinator:

Prof. Leszek Kaczmarek
http://neurogene.nencki.gov.pl
l.kaczmarek@nencki.gov.pl
Nencki Institute
Warsaw, POLAND

 

Project Manager:

Ms. Marta Rucinska
m.rucinska@nencki.gov.pl
Nencki Institute
Warsaw, POLAND

 

Recruitment Co-ordinator

Prof. Alexander Dityatev
alexander.dityatev@dzne.de
Deutsches Zentrum fur
Neurodegenerative Erkrankungen
Magdeburg, GERMANY

 

Training Co-ordinator

Prof. Robert Pawlak
R.Pawlak@exeter.ac.uk
University of Exeter Medical School
Exeter, UK

ESR3:    ECM-mediated regulation of GABAergic transmission and schizophrenia (lead: DZNE-2a, partners: MPG, NENCKI)

Gabriela Matuszko    

gabriela.matuszko@dzne.de

    Gabriela.jpg

 

 

 

 

 

 

 

The aim of this project is to create in vitro and in vivo models of neurons, which extracellular matrix is modified. In order to understand role of extracellular matrix proteins: ACAN, BCAN, HAPLN1, TN-R I use knock down AAV in two schizophrenia related brain areas: mPFC and hippocampus. Then, changes in cellular innervation and animal behavior will be analyzed. Studies of those models can help us to understand the role of extracellular matrix in schizophrenia and will give us a possibility to test how drugs preserving the extracellular matrix may help to restore normal behavior in mice.



For more information about research in the group, please see recent papers and reviews:

  • Dityatev & Rusakov (2011) Molecular signals of plasticity at the tetrapartite synapse. Curr Opin Neurobiol. 2011, 21:353-9;
  • Caiazzo et al. (2011) Direct generation of functional dopaminergic neurons from mouse and human fibroblasts. Nature 476:224-7;
  • Dityatev et al. (2010) The dual role of the extracellular matrix in synaptic plasticity and homeostasis. Nat Rev Neurosci. 11:735-46;
  • Kochlamazashvili et al. (2010) The extracellular matrix molecule hyaluronic acid regulates hippocampal synaptic plasticity by modulating postsynaptic L-type Ca2+ channels. Neuron 67:116-28.

The German Center for Neurodegenerative Diseases (DZNE) is a center of excellence within the Helmholtz Association that performs translational research on Neurodegenerative Diseases. The DZNE Magdeburg offers an excellent infrastructure in a unique research environment, with combination of animal and clinical research and in close collaboration with researchers from the Leibniz Institute for Neurobiology.

ESR3.pngHypothetical mechanism by which Tenascin-R and associated HNK-1 regulate perisomatic inhibition. The HNK-1 carried by the extracellular matrix glycoprotein tenascin-R (TN-R) interacts directly with postsynaptic GABABRs on the soma of a pyramidal neuron. This interaction inhibits the activation of GABABRs on pyramidal cells in the CA1 region of the mouse hippocampus. Genetic ablation of TN-R or application of monoclonal antibody directed against the HNK-1 carbohydrate neutralizes the inhibition of postsynaptic GABABRs by the HNK-1 carbohydrate. As a consequence, tonic GABA release activates postsynaptically both GABAARs and GABABRs. Activation of postsynaptic GABABRs elevates the rate of spontaneous asynchronous vesicle release and decreases the evoked GABA release. Reproduced from Dityatev and Schachner (2003) Nat. Rev. Neurosci. 4:456-68.