Accumulating lines of evidence have indicated that a non-selective N-methyl-d-aspartate (NMDA) receptor antagonist ketamine exerts fast and robust antidepressant effects via stimulating glutamate transmission and activating the glutamate alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors. Moreover, NMDA receptor antagonist has the ability to reduce the activity of fast-spiking (FS) interneurons which results in the disinhibition of pyramidal neurons and increases the glutamate transmission. We therefore hypothesize that FS interneurons may play an important role in the antidepressant effects of ketamine. Quantification of FS interneurons function via analyzing gamma oscillations may guide the antidepressant therapy of ketamine in clinical practice.
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