Enhancing WNT signaling restores cortical neuronal spine maturation and synaptogenesis in Tbr1 mutants.
Circuits, Cognition & Behavior
Social stimuli induce activation of oxytocin neurons within the paraventricular nucleus of the hypothalamus to promote social behavior in male mice.
Robust and replicable measurement for prepulse inhibition of the acoustic startle response.
Autism-associated Shank3 is essential for homeostatic compensation in rodent V1.
Inhibitory regulation of calcium transients in prefrontal dendritic spines is compromised by a nonsense Shank3 mutation.
Distinct pathogenic genes causing intellectual disability and autism exhibit a common neuronal network hyperactivity phenotype.
Molecular and functional characterization of circuits underlying social motivation in mouse models of autism
Humans and other animals display a strong evolutionary conserved motivation to engage in social interactions. Changes in social interactions have been observed in individuals with ASD as well as animal models of the condition. In the current project, Catherine Dulac’s laboratory aims to uncover the nature and function of neural circuits underlying social motivation in wildtype mice compared to those observed in two distinct genetic mouse models of ASD.
Interneuron transplantation rescues social behavior deficits without restoring wild-type physiology in a mouse model of autism with excessive synaptic inhibition.
Maternal experience-dependent cortical plasticity in mice is circuit- and stimulus-specific and requires MECP2.
Understanding and manipulating cortex-wide neural dynamics across multiple mouse models of autism
Autism spectrum disorder (ASD) is a complex condition associated with many different molecular and genetic causes. In the current project, Tim Buschman and colleagues aim to test the hypothesis that these different underlying causes of ASD converge to disrupt the flow of neural activity through the brain. They plan to do this by studying three different mouse models of ASD. Understanding these common disruptions and relating changes in neural activity to behavioral phenotypes will lay the foundation for improving biomarkers and treatments for ASD.
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