Procedures were developed to perform mesoscale 2-photon Ca²⁺ imaging simultaneously from all of mouse dorsolateral neocortex, facilitating identification of widespread neural ensembles with activity related to diverse aspects of behavior.

Purine recycling deficiency triggers metabolic and neurological defects reminiscent of Lesch–Nyhan disease in Drosophila, paving the way for studying this disorder and carrying out drug screening in an invertebrate organism.

Among three new models for KCNMA1 channelopathy, the most severe gain-of-function variant (Kcnma1^N999S/WT) displays a particular type of immobilizing paroxysmal dyskinesia observed in patients, including amphetamine responsiveness.

Pre-verbal infants demonstrate an implicit sensitivity to interoceptive sensations, which fluctuates spontaneously during emotional processing and guides audiovisual preferences in the environment.

Two genetically distinct Stxbp1 haploinsufficiency mouse models exhibit seizures and impairments in cognitive, psychiatric, and motor functions, representing robust preclinical models of STXBP1 encephalopathy with both construct and face validity.

A data-reduced neuro-behavioral geometry in psychosis spectrum disorders mapped symptoms stably on to distinct functional brain regions and offers a framework for informing personalized treatment selection decisions.

Perturbation of oxytocin signaling causes alterations that may be causally involved in the etiology of oxytocin-related neurobehavioral disorders.

Reactivation of paternal Ube3a by an ASO therapy in juvenile and adult mouse models of Angelman syndrome reverses the impairments of EEG power spectrum and sleep pattern, suggesting that these two core disease features may be improved by such therapies.

Transgenic mice with Rett-causing mutations in MeCP2 reveal that a basic cluster in the C-terminus of the protein binds DNA and that both the methyl-CpG binding domain and the transcriptional repression domain are necessary to elicit toxicity in MECP2 duplication syndrome.

A novel, translational mouse model of prenatal methadone exposure was developed and a longitudinal assessment of offspring revealed impairments in physical, behavioral, and neuronal development.