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Abstract #2179

Allosteric activation of mGluR4 receptor reversing social behavior deficits modifies the reward-related resting state networks in mu opioid receptor knock-out mice

Anna E. Mechling1,2, Kirsten Kleim1, Tanzil Arefin1,2, Hsu-Lei Lee1, Thomas Bienert1, Jürgen Hennig1, Dominik von Elverfeldt1, Brigitte Lina Kieffer3, and Laura-Adela Harsan1,4,5

1Medical Physics, University Medical Center Freiburg, Freiburg, Germany, 2Faculty of Biology, Albert-Ludwig-University Freiburg, Freiburg, Germany, 3Department of Psychiatry, Douglas Hospital Research Center, School of Medicine, McGill University, Montreal, QC, Canada, 4Engineering Science, Computer Science, and Imaging Laboratory, Integrative Multimodal Imaging in Healthcare, University of Strasbourg, Strasbourg, France, 5Department of Biophysics and Nuclear Medicine, University Hospital Strasbourg, Strasbourg, France

Mu opioid receptor (MOR) knock-out Oprm1-/- mice exhibit deficits in social behavior and repetitive behavior, which are phenotypes related with autism spectrum disorders (ASD). Thus, MOR deficient mice were recently proposed as monogenic models of ASD. Moreover, a decrease in metabotropic glutamate receptor 4 (mGluR4) levels was found in these mice. A treatment with VU0155041, an allosteric modulator of mGluR4, reversed behavioral deficits in Oprm1-/- mice. Here, we investigated the remodeling on brain connectivity level in Oprm1-/- mice under VU0155041-treatment and found enhancement of positive correlation towards frontal brain areas involved in reward-processing due to the compound.

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