Research: “Touchscreen Learning Deficits and Normal Social Approach Behavior in the Shank3B Model of Phelan-McDermid Syndrome and Autism”

Deletions and mutations in SHANK3 gene cause Phelan McDermid Syndrome (PMS) and have also been associated with autism spectrum disorder (ASD) and intellectual disabilities. Using a mouse model of Shank3 deletions, this study examines the hypothesis that deficits of SHANK3 expression impair brain function used in social communication and cognition. A touchscreen test used on the genetically modified mice tested the ability to be habit forming, rule following, and attentive to specific senses like hearing, seeing, and smelling. Results showed that pairwise discrimination associative learning is disrupted in heterozygous Shank3 mice for touchscreen tasks. Mutant mice were slower in visual discrimination and made more task errors. This is the first study that successfully evaluated Shank3 deletion effects using a touchscreen system, thus opening a new pathway to study the neurobiological mechanisms associated with the intellectual effects from genetic deletions and mutations in SHANK3. Further results from the study showed that null mutants (-/-) mice were not able to complete pre-training tasks—a profound deficit in intellectual ability that future studies will aim to investigate further. To read this study by researchers at the UC Davis MIND Institute, click here.

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