Susan E. Maloney

This study investigates hippocampal network dysfunction in a Wolfram syndrome mouse model, finding hyperexcitable neurons without seizures or increased network bursting.

In 136 mice on FED3 tasks, males showed slightly higher win-stay in all three choice tasks, with higher accuracy in a deterministic bandit but not a probabilistic one.

This study shows that synthetic oxytocin administered during postpartum hemorrhage prophylaxis in rats transfers via lactation and specifically suppresses neurodevelopmental risk gene networks in male offspring prefrontal cortex.

This study shows that vestibular function remains normal in Vglut3-/- mice despite severe reduction in glutamatergic synaptic transmission, suggesting non-quantal transmission compensates for the loss.

This study identifies ACSS2 as a mediator of prenatal alcohol exposure-related phenotypes, showing its role in histone acetylation and developmental changes in the brain.

This study shows that maternal separation stress disrupts noradrenergic signaling in the locus coeruleus, leading to altered coping behaviors in adulthood.

This paper introduces a homecage operant task to measure social motivation and circadian rhythms in mice, finding that social motivation peaks 2 hours after feeding and is influenced by dopamine D1 and D2 receptors.

This study examines the molecular and behavioral effects of MYT1L haploinsufficiency in mice, finding region-specific hypothalamic disruptions and sex-specific behavioral stability.

The paper shows a single binge ethanol exposure rapidly increases apoptosis in early adolescent and adult mice, with Myt1l haploinsufficiency modulating this effect across developmental stages.

This study shows that requiring mice to perform a simple action to access high-fat diet reduces intake and prevents obesity, suggesting that easy access promotes overeating.

The paper uses single-nucleus RNA-sequencing to link molecular variation in hypothalamic neurons to social motivation behavior in mice, identifying actionable targets for social deficit disorders.

This study investigates how chromosomal and gonadal sex influence social motivation in mice, finding that gonadal sex primarily affects behavior while chromosomal sex interacts with genetic mutations to alter social behavior.

This study examines the effects of Myt1l heterozygous mutation on lifespan and health in mice, finding no significant difference in lifespan or end-of-life histopathology compared to wildtype mice.

This study shows that Astn2 knockout mice display ASD-like behaviors and altered cerebellar circuit properties, including changes in synaptic transmission and glial volume.

This study examines how different DNMT3A mutations cause varied behavioral, epigenetic, and transcriptional issues in neurodevelopmental disorders.

This study examines functional connectivity changes in Mecp2 knockout mice, finding disrupted connectivity in males and subtle changes in females, suggesting sex-specific roles of MeCP2 in circuit development.

This study compares long-term effects of in utero versus continued postnatal oxycodone exposure in mice, finding sex-dependent changes in sensory and reward processing but no major behavioral deficits.

This paper develops a MYT1L syndrome mouse model that recapitulates human phenotypes, revealing disrupted brain development and neuronal maturation as underlying mechanisms.

This study uses iPSC models to show that a 15q13.3 duplication causes distinct neurodevelopmental and functional anomalies in an affected individual but not their unaffected mother, while both share increased cholinergic activity.

This study examines the effects of in utero and postnatal oxycodone exposure on mouse behavior and development, finding sex-dependent weight changes, altered vocalizations, and sensorimotor delays.

This study shows that transient placental ischemia-hypoxemia in pregnant rats causes oxidative stress and long-term mitochondrial and behavioral issues in male offspring.

This study identifies genomic binding sites of Gtf2i and Gtf2ird1 in the developing brain and assesses their combined effects on transcription and behavior in knockout mice.

The paper shows astrocytes have a translational response to neuronal activity, altering their proteome at synapses through BDNF and K+ signals.

The paper uses CRISPR TRAPseq to show QKI is important for astrocytic maturation and synaptic control in vivo.

This study shows that maternal SSRI exposure during offspring development causes long-term behavioral, cellular, and neuroimaging disruptions, suggesting a direct role in ASD risk.