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DA pathways in the BG are important for motor, emotional, and cognitive function. The changes in DA signaling and striatal circuitry observed in 16p11+/? mice suggest possible mechanisms relevant for deficits observed in 16p11.2 deletion syndrome. We therefore tested 16p11+/? mice in a battery of behaviors to assay defects in locomotor activity, social interaction, working memory, and sensory processing. To control for variability across testing sites, these studies were conducted in parallel by the Stanford Behavioral and Functional Neuroscience Laboratory (SBFNL) and by the Laboratory of Behavioral Neuroscience at the National Institute of Mental Health (NIMH). Tests were performed on increasing C57BL/6N background after hybrid founder mice Rucaparib concentration had been backcrossed into C57BL/6N for at least five to seven times. ALK inhibitor clinical trial Eight- to 12-week-old 16p11+/? mice did not show gross defects in a battery of tests for general health and neurological reflexes ( Tables S3 and S4; Figure?S6A). The mice also had normal olfactory abilities, as assessed in the olfactory habituation/dishabituation test ( Figure?S6B), and normal vision, as assessed by the forepaw reaching test ( Table S3). However, 16p11+/? mice lacked a startle response even to sounds at 120 dB (NIMH: at 100 dB, F1,30?= 8.04, p?Fluconazole gait (wild-type: 19.4%, 16p11+/?: 52.8, p?