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. Mechling^1,2, Kirsten Kleim¹, Tanzil Arefin^1,2, Hsu-Lei Lee¹, Thomas Bienert¹, Jürgen Hennig¹, Dominik von Elverfeldt¹, Brigitte Lina Kieffer³, and Laura-Adela Harsan^1,4,5

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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