Common circuit defect of excitatory-inhibitory balance in mouse models of autism.
Gogolla N, Leblanc JJ, Quast KB, Südhof TC, Fagiolini M, Hensch TK. · 2009
Read Common circuit defect of excitatory-inhibitory balance in mouse models of autism. by Gogolla N, Leblanc JJ, Quast KB, Südhof TC, Fagiolini M, Hensch TK. (2009) in the Tower of Babel, a free online library of public-domain works preserved in clean, searchable text. No sign-up. The full text is served as a plain-text file at a predictable URL, where text is present: https://antarctic-labs.com/tower-of-babel/europmc-pmc2906812.txt.
Description
Gogolla and colleagues hunted in 2009 for one shared circuit flaw across the many mouse models of autism, a condition with dozens of unrelated genetic and environmental causes. A leading theory blames imbalance between excitatory and inhibitory signaling during development. The team focused on parvalbumin-positive inhibitory neurons, the cells that pace cortical circuits and drive their experience-based refinement.
Pooling published models, they found these inhibitory cells reduced in the neocortex again and again. They also tested two more models. One was exposed before birth to the drug valproate, and one carried a human autism mutation. In the two new models the loss was lopsided between brain hemispheres in vision and touch areas, but spared a memory structure nearby. A common circuit defect amid diverse causes suggests prevention might target the shared pathway.
Catalog record
| CREATOR | Gogolla N, Leblanc JJ, Quast KB, Südhof TC, Fagiolini M, Hensch TK. |
|---|---|
| YEAR | 2009 |
| COLLECTION | PAPERS |
| FORMAT | TXT |
| FILE SIZE | 47 KB |
| LICENSE | CC BY 4.0 |
| RIGHTS | CC BY |
| SOURCE | Europe PMC |