Testing the excitation/inhibition imbalance hypothesis in a mouse model of the autism spectrum disorder: in vivo neurospectroscopy and molecular evidence for regional phenotypes.
Joana Gonçalves, Inês R Violante, José Sereno and 6 others
PMID 28932379WHAT IT FOUND
In mice modelling NF1, brain imbalance differed by region: prefrontal and striatal circuits showed more inhibitory GABA relative to glutamate, while hippocampus showed more GABA receptors despite lower GABA.
This was not a therapy test.
Key findings
01In mutant mice, the balance of inhibitory GABA relative to excitatory glutamate was higher in prefrontal cortex and striatum, but not hippocampus.
02Mutant mice had lower hippocampal GABA and lower glutamate in hippocampus and striatum.
03Hippocampal GABA(A) receptor protein was higher, prefrontal receptor protein was lower, and striatal receptor protein was unchanged in mutant mice.
STILL TO COME
How it was doneWhat they found
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What it does not show
This was a mouse study, so it does not show what happens in human patients. It tested only one genetic model, NF1, not autism spectrum disorder generally. The sample was small: 14 mutant mice and 13 control mice. It measured brain chemistry and receptor expression, not behaviour, therapy response, or patient outcomes. The authors note that mouse and human NF1 findings did not match in all brain regions.
The easy way to misread this
Do not conclude that correcting excitation/inhibition imbalance in autism has been shown to work. This study only measured brain chemistry in mice with an NF1 mutation and tested no therapy.