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- W2800955338 abstract "Summary Distinct genetic forms of autism are hypothesized to share a common increase in excitation-inhibition (E-I) ratio in cerebral cortex, causing hyperexcitability and excess spiking. We provide the first systematic test of this hypothesis across 4 mouse models ( Fmr1 −/y , Cntnap2 −/- , 16p11.2 del/+ , Tsc2 +/- ), focusing on somatosensory cortex. All autism mutants showed reduced feedforward inhibition in layer 2/3 coupled with more modest, variable reductions in feedforward excitation, driving a common increase in E-I conductance ratio. Despite this, feedforward spiking, synaptic depolarization and spontaneous spiking were essentially normal. Modeling revealed that E and I conductance changes in each mutant were quantitatively matched to yield stable, not increased, synaptic depolarization for cells near spike threshold. Correspondingly, whisker-evoked spiking was not increased in vivo , despite detectably reduced inhibition. Thus, elevated E-I ratio is a common circuit phenotype, but appears to reflect homeostatic stabilization of synaptic drive, rather than driving network hyperexcitability in autism." @default.
- W2800955338 created "2018-05-17" @default.
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- W2800955338 date "2018-05-09" @default.
- W2800955338 modified "2023-09-30" @default.
- W2800955338 title "Increased excitation-inhibition ratio stabilizes synapse and circuit excitability in four autism mouse models" @default.
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- W2800955338 doi "https://doi.org/10.1101/317693" @default.
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