ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Altered Neural Activity in the Mesoaccumbens Pathway Underlies Impaired Social Reward Processing in Shank3-Deficient Rats.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- AAV-only targeting of ventral tegmental area dopamine neurons for optical self-stimulation studies in mice.Scientific reports · 2026Article
- Midbrain endocannabinoids actuate dopamine-based action selection.Cell reports · 2026Article
- Remimazolam Ameliorates Autistic-Like Behaviors via Suppression of Ferroptosis in VTA Dopaminergic Neurons in a Mouse Model of ASD.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Prenatal valproate exposure alters midbrain and striatal neuronal morphology along with dopamine levels.Brain structure & function · 2026Article
- AAV-only targeting of ventral tegmental area dopamine neurons for optical self-stimulation studies in mice.bioRxiv : the preprint server for biology · 2026Article
- Altered Neural Activity in the Mesoaccumbens Pathway Underlies Impaired Social Reward Processing in Shank3-Deficient Rats.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Juvenile social isolation in Sprague Dawley rats does not have a lasting impact on social behavior in adulthood.Scientific reports · 2025Article
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Abstract
Social behaviors are crucial for human connection and belonging, often impacted by conditions like Autism Spectrum Disorder (ASD). The mesoaccumbens pathway (ventral tegmental area (VTA) to the nucleus accumbense (NAc)) plays a pivotal role in social behavior and is implicated in ASD. However, the impact of ASD-related mutations on social reward processing remains insufficiently explored. This study focuses on the Shank3 mutation, associated with a rare genetic condition and linked to ASD, examining its influence on the mesoaccumbens pathway during behavior, using the Shank3-deficient rat model. Our findings indicate that Shank3-deficient rats exhibit atypical social interactions, associated with altered neuronal activity of VTA dopaminergic and GABAergic neurons and reduced dopamine release in the NAc. Moreover, they demonstrate that manipulating VTA neuronal activity can normalize this behavior, providing insights into the effects of Shank3 mutations on social reward processing and identifying a potential neural pathway for intervention.
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