Speaker: Sara Kornfeld-Sylla (Bear Lab) 

Title: A human electrophysiological signature of Fragile X pathophysiology is shared in V1 of Fmr1-/y mice

Abstract: Predicting clinical therapeutic outcomes from animal studies using conserved electrophysiological phenotypes could facilitate developing treatments for neuropsychiatric disorders. Alpha oscillations in human resting-state electroencephalogram recordings are altered in many disorders, but whether these disruptions exist in mouse models is unknown. We employ a uniform analytical method to show in males with fragile X syndrome (FXS) that alpha oscillations in humans and alpha-like oscillations in visual cortex of Fmr1-/y mice are slowed, with a stronger phenotype in adults than juveniles and a juvenile-specific power phenotype in both species. We also find that alpha-like oscillations are more sensitive to activation of GABAB receptors by Arbaclofen in wild-type than Fmr1-/y mice. Our framework reveals evolutionary conservation of alpha oscillation disruptions, enables deeper understanding of FXS pathophysiology, and narrows the gap between treatment promise and practice.

Speaker: Matias Andina (Choi/Hrvatin Lab) 

Title: Wiring the Torpor Switch: AgRP Circuit Control of Energy Saving

Abstract:Torpor is a survival strategy used during energy shortage. It is marked by reduced body temperature, inactivity, and lower metabolic rate. In mice, fasting-induced torpor depends on a hypothalamic circuit linking AgRP neurons in the arcuate nucleus to preoptic neurons in the MnPO. This pathway helps convey energy-state information to thermoregulatory centers.Disrupting the circuit prevents torpor during fasting, indicating a central role in energy conservation. NPY and GABA signaling from AgRP neurons also contribute to starvation-induced hypothermic responses.