communication impairments in mice lacking shank1 reduced levels of ultrasonic vocalizations and scent marking behavior沟通障碍小鼠缺乏shank1减少超声波声音和气味标记行为的水平.pdf

Communication Impairments in Mice Lacking Shank1: Reduced Levels of Ultrasonic Vocalizations and Scent Marking Behavior ¨ 1 ¤ 1 2 2 1 Markus Wohr * , Florence I. Roullet , Albert Y. Hung , Morgan Sheng , Jacqueline N. Crawley * 1 Laboratory of Behavioral Neuroscience, National Institute of Mental Health, Bethesda, Maryland, United States of America, 2 The Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America Abstract Autism is a neurodevelopmental disorder with a strong genetic component. Core symptoms are abnormal reciprocal social interactions, qualitative impairments in communication, and repetitive and stereotyped patterns of behavior with restricted interests. Candidate genes for autism include the SHANK gene family, as mutations in SHANK2 and SHANK3 have been detected in several autistic individuals. SHANK genes code for a family of scaffolding proteins located in the postsynaptic density of excitatory synapses. To test the hypothesis that a mutation in SHANK1 contributes to the symptoms of autism, we evaluated Shank1 2/ 2 null mutant mice for behavioral phenotypes with relevance to autism, focusing on social communication. Ultrasonic vocalizations and the deposition of scent marks appear to be two major modes of mouse communication. Our findings revealed evidence for low levels of ultrasonic vocalizations and scent marks in Shank12/ 2 mice as compared to wildtype Shank1+/+ littermate controls. Shank12/ 2 pups emitted fewer vocalizations than Shank1+/+ pups when isolated from mother and littermates. In adulthood, genotype affected scent marking be