Abstract
Animal models, and previous magnetic resonance spectroscopy (1HMRS) studies in humans suggest excitatory glutamatergic and inhibitory gamma-aminobutyric acid (GABA)-ergic neurotransmission contributes to the fast-acting antidepressant effects of treatments such as ECT. Here, we addressed whether changes in glutamate (Glu) and GABA levels associate with the rapid therapeutic effects of ketamine, a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist, in patients with major depression.
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