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ETRABRAIN EU FP7 - Initial Training Network | ESR3

Project Co-ordinator:

Prof. Leszek Kaczmarek
Nencki Institute
Warsaw, POLAND


Project Manager:

Ms. Marta Rucinska
Nencki Institute
Warsaw, POLAND


Recruitment Co-ordinator

Prof. Alexander Dityatev
Deutsches Zentrum fur
Neurodegenerative Erkrankungen
Magdeburg, GERMANY


Training Co-ordinator

Prof. Robert Pawlak
University of Exeter Medical School
Exeter, UK

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

Gabriela Matuszko    










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.

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