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So, the researchers also implanted a microdialysis catheter, effectively allowing them to see what neurotransmitters were released and at roughly what time

J Clin Endocrinol Metab 77:13841387

Mitochondrial dysfunction could not be compensated by increasing oxidative phosphorylation, so that it was only compensated by activating the glycolytic pathway, which was inefficient at producing ATP (18)

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It may act by increasing gamma-aminobutyric acid levels in the brain or by altering the properties of voltage-gated sodium channels