Social Novelty Recruits
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Social Novelty Recruits a Dysfunctional Nucleus Accumbens Ensemble That Drives Social Avoidance in a Shank3-/- Autism Model
Social behavior deficits are a common symptom of neuropsychiatric disorders, including autism spectrum disorder (ASD), but there are limited pharmacological treatments for these symptoms. Understanding how neurons encode social information will give insight into identifying novel pharmacological targets to address this unmet need. SHANK3 encodes a postsynaptic scaffold protein and is a common risk gene for several neuropsychiatric disorders characterized by social deficits, including ASD.