Abstract
Genetically modified mice shed new light on how ketamine can target NMDA receptors in the brain to reduce the symptoms of depression.
Highlights
Studies have shown that blocking N-methyl-D aspartate receptor (NMDAR) proteins with ketamine reverses depressive-like behavior more quickly and more effectively than traditional antidepressant medications (Zarate et al, 2006; Li et al, 2010; Autry et al, 2011)
The 2BΔCtx mice had higher levels of excitatory activity in the prefrontal cortex of the brain, and ketamine—which increased excitatory activity in the wild-type mice—had no additional effect. These results indicate that the antidepressant action of ketamine may be caused by the changes in the excitation of neurons
Using a method of protein tagging called FUNCAT— which makes it possible to see when proteins are being made (Dieterich et al, 2010)—they confirmed that there is an increase in the baseline levels of protein synthesis in neurons from 2BΔCtx mice compared to neurons from wild-type mice
Summary
Studies have shown that blocking NMDAR proteins with ketamine reverses depressive-like behavior more quickly and more effectively than traditional antidepressant medications (Zarate et al, 2006; Li et al, 2010; Autry et al, 2011). It has similar effects to drugs that block one of the subunits of the NMDAR protein, known as GluN2B (Li et al, 2010).
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