GABAergic neurons exhibit subtype-specific changes in the developing somatosensory cortex of a rat model of Fragile X Syndrome

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 expression patterns are regulated in early development across other mammalian models fo FXS. Here we utilise an outbred rat model of FXS, in which we performed single-nucleus RNA sequencing analysis in neonatal development of the somatosensory cortex. We then use immunohistochemistry to measure the number and distribution of neurochemically identified GABAergic IN subtypes from early development until adolescence in the somatosensory cortex.