Cellular mechanisms underlying the antidepressant effects of ketamine: role of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptors.

By S. Maeng, C. Zarate, Jing Du, R. Schloesser, Joseph McCammon, Guang Chen, Husseini K. Manji. Biological Psychiatry, 2008

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Towards a glutamate hypothesis of depression (2011, background): “…providing some insight into the mechanism of antidepressant action, recent studies suggest the antidepressant-like effects of ketamine and other NMDA antagonists may be dependent on enhancement of AMPA-R activation (Autry et al., 2011; Koike et al., 2011; Li et al., 2010; Maeng et al., 2008).”
Targeting the glutamatergic system to develop novel, improved therapeutics for mood disorders (2008, background): “The ability to block ketamine's antidepressant-like effects with an AMPA antagonist suggests that enhanced AMPA throughput might be crucial in producing these effect”
Glutamate NMDA receptor antagonists rapidly reverse behavioral and synaptic deficits caused by chronic stress exposure (2011, positive): “A previous study has reported that the behavioral actions of Ro 25-6981 in the FST do not persist as long as ketamine (7).”
A Randomized Add-on Trial of an N-methyl-d-aspartate Antagonist in Treatment-Resistant Bipolar Depression (2010, neutral): “Lithium 7 (39) 16 (89) Antidepressants Duloxetine 7 (39) 13 (72) SSRI 6 (33) 18 (100) Bupropion 5 (28) 16 (89) Venlafaxine 2 (11) 11 (61) Trazodone 2 (11) 7 (39) MAOI 1 (6) 7 (39) TCA 0 7 (39) Mirtazapine 0 6 (33) Nefazodone 0 3 (17) Antipsychotics Quetiapine 9 (50) 16 (89) Aripiprazole 2 (11) 10 (5”