Journal
MOLECULAR PSYCHIATRY
Volume 24, Issue 9, Pages 1248-1257Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41380-019-0426-0
Keywords
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Funding
- NIMH [R01 MH100292, R01 MH106507, R01 MH081880, R37 MH049428]
- Simons Foundation (SFARI) [309279]
- NINDS [R01 NS34661]
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In 2003 Rubenstein and Merzenich hypothesized that some forms of Autism (ASD) might be caused by a reduction in signal-to-noise in key neural circuits, which could be the result of changes in excitatory-inhibitory (E-I) balance. Here, we have clarified the concept of E-I balance, and updated the original hypothesis in light of the field's increasingly sophisticated understanding of neuronal circuits. We discuss how specific developmental mechanisms, which reduce inhibition, affect cortical and hippocampal functions. After describing how mutations of some ASD genes disrupt inhibition in mice, we close by suggesting that E-I balance represents an organizing framework for understanding findings related to pathophysiology and for identifying appropriate treatments.
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