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Acute low-dose ketamine produces a rapid and robust increase in plasma BDNF without altering brain BDNF concentrations.

Martin Le Nedelec, Paul Glue, Helen Winter, Chelsea Goulton, Lucy Broughton, Natalie J. Medlicott

Drug delivery and translational research June 2018 DOI: 10.1007/s13346-017-0476-2 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Preclinical experimental study Peer reviewed
Population Rats
Intervention Ketamine
Dose 10 mg/kg
Duration 240 min
Topics Ketamine Esketamine
Keywords Bdnf Biomarker Major depression Treatment resistant
Key findings A single 10 mg/kg ketamine dose produced a rapid, sustained (240-minute) increase in plasma BDNF in rats, but no changes in brain BDNF in prefrontal cortex, hippocampus, or cortex, and no correlation between peripheral and central BDNF. The authors suggest peripheral BDNF is unlikely to be a useful biomarker of acute central BDNF changes after ketamine.

Abstract

Peripheral BDNF changes after ketamine administration have been proposed as a biomarker for brain BDNF changes. However, published data are conflicting and come from studies in paired animal groups. This study determined the time course of plasma BDNF concentrations following the administration of a single 10 mg/kg dose of ketamine by different routes of administration in rats. Brain BDNF concentrations in prefrontal cortex, hippocampus and cortex were measured in the same animals. Ketamine administration resulted in a rapid and robust increase in plasma BDNF concentrations that were sustained for 240 min. In contrast, there were no changes in brain BDNF concentrations in prefrontal cortex, hippocampus or cortex and there were no correlations between peripheral and central BDNF concentrations. These data suggest that peripheral BDNF is unlikely to be a useful biomarker of acute central BDNF changes following ketamine.

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