| First Author | Goel A | Year | 2018 |
| Journal | Nat Neurosci | Volume | 21 |
| Issue | 10 | Pages | 1404-1411 |
| PubMed ID | 30250263 | Mgi Jnum | J:267057 |
| Mgi Id | MGI:6257311 | Doi | 10.1038/s41593-018-0231-0 |
| Citation | Goel A, et al. (2018) Impaired perceptual learning in a mouse model of Fragile X syndrome is mediated by parvalbumin neuron dysfunction and is reversible. Nat Neurosci 21(10):1404-1411 |
| abstractText | To uncover the circuit-level alterations that underlie atypical sensory processing associated with autism, we adopted a symptom-to-circuit approach in the Fmr1-knockout (Fmr1(-/-)) mouse model of Fragile X syndrome. Using a go/no-go task and in vivo two-photon calcium imaging, we find that impaired visual discrimination in Fmr1(-/-) mice correlates with marked deficits in orientation tuning of principal neurons and with a decrease in the activity of parvalbumin interneurons in primary visual cortex. Restoring visually evoked activity in parvalbumin cells in Fmr1(-/-) mice with a chemogenetic strategy using designer receptors exclusively activated by designer drugs was sufficient to rescue their behavioral performance. Strikingly, human subjects with Fragile X syndrome exhibit impairments in visual discrimination similar to those in Fmr1(-/-) mice. These results suggest that manipulating inhibition may help sensory processing in Fragile X syndrome. |
