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Ketamine induces behavioral and neural effects that can present differently in healthy volunteers (HV), major depressive disorder (MDD), or treatment-resistant depression (TRD). When infused at an antidepressant dose of 0.5 mg/kg, ketamine manifests psychoactive effects in HV, MDD, and TRD. Depressed ketamine responders usually experience a reduction in symptoms within hours to days after infusion, whereas non-responders do not. The effects of ketamine on electroencephalography (EEG) and functional connectivity (FC) often differ between HV and depressed patients. In depression, ketamine can “normalize” FC to the levels of HV receiving placebo, but FC may also be altered differently. Sometimes ketamine-induced changes in FC correlate with antidepressant relief. No universal biomarker has been established, but in longitudinal observation, ketamine consistently increases EEG gamma power in frontoparietal regions, FC within prefrontal cortex, and functional striatal activation. Limited data report similar ketamine effects in HV and non-responders. Differences between depressed patients and HV are observed for weeks after ketamine exposure. The effects of ketamine on HV cannot be directly extrapolated to MDD, TRD, or remitters. Individual experience, anxiety, and psychological and physiological conditions can influence ketamine’s effects on patients and HV.

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Patients and Healthy Volunteers Are Not the Same: The Distinct Responses to Ketamine

  • 实验方案

  • 发表日期：

    2025年

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  • Sabine Himmelseher,
  • Eberhard F. Kochs

摘要

Ketamine induces behavioral and neural effects that can present differently in healthy volunteers (HV), major depressive disorder (MDD), or treatment-resistant depression (TRD). When infused at an antidepressant dose of 0.5 mg/kg, ketamine manifests psychoactive effects in HV, MDD, and TRD. Depressed ketamine responders usually experience a reduction in symptoms within hours to days after infusion, whereas non-responders do not. The effects of ketamine on electroencephalography (EEG) and functional connectivity (FC) often differ between HV and depressed patients. In depression, ketamine can “normalize” FC to the levels of HV receiving placebo, but FC may also be altered differently. Sometimes ketamine-induced changes in FC correlate with antidepressant relief. No universal biomarker has been established, but in longitudinal observation, ketamine consistently increases EEG gamma power in frontoparietal regions, FC within prefrontal cortex, and functional striatal activation. Limited data report similar ketamine effects in HV and non-responders. Differences between depressed patients and HV are observed for weeks after ketamine exposure. The effects of ketamine on HV cannot be directly extrapolated to MDD, TRD, or remitters. Individual experience, anxiety, and psychological and physiological conditions can influence ketamine’s effects on patients and HV.