Dan Feldman, a professor at the University of California, Berkeley, studies the rodent somatosensory cortex, which is famous for its organized groupings of neurons, called ”barrels.” There, his lab has been testing an influential idea about autism: the excitatory-inhibitory (E-I) imbalance hypothesis. This proposes that an excess of excitatory signaling relative to inhibitory signaling in the brain leads to symptoms of autism.
In a recent paper, Feldman’s lab found evidence for the E-I imbalance hypothesis, but not exactly in the way many expected: the changes appeared to reflect a compensation for some other problem in the circuit, rather than a primary deficit causing circuit hyperexcitability. I recently spoke with Feldman to discuss these findings and what they might mean for therapeutic approaches aimed at restoring inhibition in autism.
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