Atypical sensory processing occurs in a majority of individuals with Fragile X syndrome (FXS), the leading inherited cause of autism. Our lab recently discovered that Fmr1 knockout (Fmr1-/-) mice, a model of FXS, manifest avoidance behaviors in response to repetitive tactile stimuli, as well as delayed perceptual learning of a visual discrimination task. At the circuit level, we found that hypoactivity of GABAergic parvalbumin interneurons (PV-INs) in the mutant mice in somatosensory and visual cortices. This hypofunction of PV interneurons begins at very early developmental stages in Fmr1-/- mice. Approaches that increase PV cell firing in Fmr1-/- mice could restore circuit function.

Host: Sam Kwon

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