NMDA receptor blockade at rest triggers rapid behavioural antidepressant responses

Anita E. Autry, Megumi Adachi, Elena Nosyreva, Elisa S. Na, Maarten F. Los, Peng-fei Cheng, Ege T. Kavalali () and Lisa M. Monteggia ()
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Anita E. Autry: University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard
Megumi Adachi: University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard
Elena Nosyreva: University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard
Elisa S. Na: University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard
Maarten F. Los: University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard
Peng-fei Cheng: University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard
Ege T. Kavalali: University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard
Lisa M. Monteggia: University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard

Nature, 2011, vol. 475, issue 7354, 91-95

Abstract: Route to fast antidepressants? Antidepressants such as selective serotonin re-uptake inhibitors can take months to take effect, but small doses of ketamine, a glutamatergic N-methyl-D-aspartate receptor (NMDAR) agonist, can have antidepressant effects within hours. The antidepressant mechanism of ketamine is not well understood. Work in mice shows that antidepressant-like effects of ketamine depend on rapid synthesis of brain-derived neurotrophic factor (BDNF). Ketamine-mediated NMDAR blockade deactivates eukaryotic elongation factor 2 (eEF2) kinase, resulting in reduced eEF2 phosphorylation and de-suppression of BDNF translation. These findings raise the possibility of this pathway as a therapeutic target for fast-acting antidepressants.

Date: 2011
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DOI: 10.1038/nature10130

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