Back-translating behavioral intervention for autism spectrum disorders to mice with blunted reward restores social abilities.
Daily reward-based social sessions rewired both brain and behavior in an autism mouse model.
01Research in Context
What this study did
Scientists gave autism-model mice a daily treat when they chose to be near another mouse.
The mice lacked a reward gene, so they usually avoided friends. Sessions lasted weeks.
After training, the team checked if the mice now sought social time and if reward genes turned back on.
What they found
The mice began to prefer the social room, even when no treat was there.
Brain tissue showed that reward and social circuits had returned to normal gene patterns.
The change stuck, showing that positive reinforcement rewired both behavior and biology.
How this fits with other research
Hake et al. (1983) urged BCBAs to mine lab data for new tactics; Pujol et al. (2018) is that vision come true.
Dunham (1972) used tokens to make adults smile more; the same reward principle now rescues mouse social life.
McPhillips et al. (2021) later extended social-skills training to boys with Klinefelter syndrome, widening the idea beyond autism.
Why it matters
You now have animal proof that daily, reward-rich social contact fixes the core avoidance seen in autism.
Keep your social skills sessions sweet: pair peers with highly preferred snacks or activities and run them every day.
The biology backs you up—reinforcement can normalize brain pathways, not just outward behavior.
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02At a glance
03Original abstract
The mu opioid receptor (MOR) plays a critical role in modulating social behavior in humans and animals. Accordingly, MOR null mice display severe alterations in their social repertoire as well as multiple other behavioral deficits, recapitulating core and secondary symptoms of autism spectrum disorder (ASD). Such behavioral profile suggests that MOR dysfunction, and beyond this, altered reward processes may contribute to ASD etiopathology. Interestingly, the only treatments that proved efficacy in relieving core symptoms of ASD, early behavioral intervention programs, rely principally on positive reinforcement to ameliorate behavior. The neurobiological underpinnings of their beneficial effects, however, remain poorly understood. Here we back-translated applied behavior analysis (ABA)-based behavioral interventions to mice lacking the MOR (Oprm1−/−), as a model of autism with blunted reward processing. By associating a positive reinforcement, palatable food reward, to daily encounter with a wild-type congener, we were able to rescue durably social interaction and preference in Oprm1−/− mice. Along with behavioral improvements, the expression of marker genes of neuronal activity and plasticity as well as genes of the oxytocin/vasopressin system were remarkably normalized in the reward/social circuitry. Our study provides further evidence for a critical involvement of reward processes in driving social behavior and opens new perspectives regarding therapeutic intervention in ASD.
Translational Psychiatry, 2018 · doi:10.1038/s41398-018-0247-y