Social circuit: Social behaviors are differentially modulated by distinct neuron types in the nucleus accumbens, according to a new study in a mouse model of autism. D1-dopamine receptor-containing medium spiny neurons promote sociability in mice missing the autism-linked CNTNAP2 gene, whereas D2-containing neurons suppress the behavior. Further, selectively inhibiting D2-containing neurons increased social interaction in the knockout mice, “providing proof of principle that targeted modulation of nucleus accumbens circuit activity can ameliorate social deficits,” the authors write.
Autism research spotted this week:
- “Autism spectrum disorder and life expectancy among Medicaid beneficiaries” JAMA Network Open
- “EEG resting-state gamma power as a potential biomarker of excitation / inhibition imbalance in autism: Evidence from the Autism Biomarkers Consortium for Clinical Trials” European Neuropsychopharmacology
- “Characterizing features of the genetic architecture underlying autism from a multi-ancestry perspective” Molecular Psychiatry
See also: “Familiar autism-linked genes emerge from first analysis of Latin American cohort” - “Excitation/inhibition balance subtypes in autism and their genetic, neural, and clinical profiles” Journal of Neural Transmission
- “Common genetic variants are associated with increased likelihood of latent co-occurring neurodevelopmental and mental health factors among autistic individuals” Molecular Psychiatry
- “Cumulative incidence and prevalence of autism spectrum disorder” JAMA Pediatrics
- “Leveraging scalable non-mammalian systems for large-scale studies of autism risk gene function” Biological Psychiatry
