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Researchers dispute the therapeutic mode of action of a ketamine metabolite

A study in Nature contradicts a previous report on synaptic NMDAR inhibition by a ketamine metabolite, a potential antidepressant.

Illustration of brain synapse


In a new study, researchers studied the effect of the ketamine metabolite on directly measured synaptic currents in vivo.

Scientists are trying to develop treatments that harness the rapid depression-relieving effects of ketamine without the risk of unwanted side effects, such as hallucinations and loss of memory.

Previous research in mice found that a ketamine metabolite, known as (2R,6R)-HNK, can exert antidepressive effects similar to ketamine independently of the synaptic N-methyl-D-aspartate receptor (NMDAR) and that this might result in fewer side effects.

In a new study, researchers studied the effect of the metabolite on directly measured synaptic currents in vivo. Using a higher dose than that explored by the other researchers, they showed that the metabolite does block the NMDAR, resulting in a downstream cascade that has been reported responsible for the antidepressant effects of ketamine.

Reporting in Nature[1] (online, 21 June 2017), the team say their findings contradict those of their colleagues and indicate that blocking NMDAR is likely to be the mechanism by which (2R,6R)-HNK exerts its long-lasting antidepressant effects.

Citation: Clinical Pharmacist DOI: 10.1211/CP.2017.20203196

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