IntroductionGABAergic interneurons (IN) are critical for the precise timing and flow of information in cortical circuits. Loss of GABAergic IN function has been suggested as a potential translationally relevant mechanism of neuropathology in Fragile X Syndrome (FXS). Indeed, in rodent models of FXS, some IN populations may display reduced number, while genes associated with other IN type upregulated. However, it remains unknown how these cell populations, and their cell-type specific gene expres
GABAergic neurons exhibit subtype-specific changes in the developing somatosensory cortex of a rat model of Fragile X Syndrome
Sam A. Booker
