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Neuronal signature of social novelty exploration in the VTA: implication for Autism Spectrum Disorder

Sebastiano Bariselli, Hanna Hörnberg, Clément Prévost-Solié, Stefano Musardo, Laetitia Hatstatt-Burkle, Peter Scheiffele, View ORCID ProfileCamilla Bellone
doi: https://doi.org/10.1101/280537
Sebastiano Bariselli
1Department of Basic Neurosciences, University of Geneva, 1211 Geneva, Switzerland
3Department of Fundamental Neurosciences, University of Lausanne, 1005 Lausanne, Switzerland
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Hanna Hörnberg
2Biozentrum of the University of Basel, 4056 Basel, Switzerland
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Clément Prévost-Solié
1Department of Basic Neurosciences, University of Geneva, 1211 Geneva, Switzerland
3Department of Fundamental Neurosciences, University of Lausanne, 1005 Lausanne, Switzerland
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Stefano Musardo
1Department of Basic Neurosciences, University of Geneva, 1211 Geneva, Switzerland
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Laetitia Hatstatt-Burkle
2Biozentrum of the University of Basel, 4056 Basel, Switzerland
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Peter Scheiffele
2Biozentrum of the University of Basel, 4056 Basel, Switzerland
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Camilla Bellone
1Department of Basic Neurosciences, University of Geneva, 1211 Geneva, Switzerland
3Department of Fundamental Neurosciences, University of Lausanne, 1005 Lausanne, Switzerland
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  • ORCID record for Camilla Bellone
  • For correspondence: Camilla.Bellone@unige.ch
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Abstract

Novel stimuli attract our attention, promote exploratory behavior, and facilitate learning. Atypical habituation and aberrant novelty exploration have been related with the severity of Autism Spectrum Disorders (ASD) but the underlying neuronal circuits are unknown. Here, we report that dopamine (DA) neurons of the ventral tegmental area (VTA) promote the behavioral responses to novel social stimuli, support preference for social novelty, and mediate the reinforcing properties of novel social interaction. Social novelty exploration is associated with the insertion of calcium-permeable GluA2-lacking AMPA-type glutamate receptors at excitatory synapses on VTA DA neurons. These novelty-dependent synaptic adaptations only persist upon repeated exposure to social stimuli and sustain social interaction. Global or DA neuron-specific inactivation of the ASD risk gene Neuroligin3 alters both social novelty exploration and the reinforcing properties of social stimuli. These behavioral deficits are accompanied by an aberrant expression of non-canonical GluA2-lacking AMPA-receptors at excitatory synapses on VTA DA neurons and an occlusion of novelty-induced synaptic plasticity. Altogether, these findings causally link impaired novelty exploration in an ASD mouse model to VTA DA circuit dysfunction.

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Posted March 12, 2018.
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Neuronal signature of social novelty exploration in the VTA: implication for Autism Spectrum Disorder
Sebastiano Bariselli, Hanna Hörnberg, Clément Prévost-Solié, Stefano Musardo, Laetitia Hatstatt-Burkle, Peter Scheiffele, Camilla Bellone
bioRxiv 280537; doi: https://doi.org/10.1101/280537
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Neuronal signature of social novelty exploration in the VTA: implication for Autism Spectrum Disorder
Sebastiano Bariselli, Hanna Hörnberg, Clément Prévost-Solié, Stefano Musardo, Laetitia Hatstatt-Burkle, Peter Scheiffele, Camilla Bellone
bioRxiv 280537; doi: https://doi.org/10.1101/280537

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