16p11.2 deletion mice display cognitive deficits in touchscreen learning and novelty recognition tasks.
16p11.2 deletion syndrome mice display sensory and ultrasonic vocalization deficits during social interactions.
Behavioral abnormalities and circuit defects in the basal ganglia of a mouse model of 16p11.2 deletion syndrome.
Communication impairments in mice lacking Shank1: reduced levels of ultrasonic vocalizations and scent marking behavior.
Haploinsufficiency of the autism-associated SHANK3 gene leads to deficits in synaptic function, social interaction, and social communication.
CHD8 mutation leads to autistic-like behaviors and impaired striatal circuits.
Dominant-negative SMARCA4 mutants alter the accessibility landscape of tissue-unrestricted enhancers.
R-baclofen reverses cognitive deficits and improves social interactions in two lines of 16p11.2 deletion mice.
Impaired perceptual learning in a mouse model of fragile X syndrome is mediated by parvalbumin neuron dysfunction and is reversible.
Characterization of medication use in a multicenter sample of pediatric inpatients with autism spectrum disorder.
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