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The Ketamine Model of the Near-Death Experience: A Central Role for the N-Methyl-D-Aspartate Receptor

K. Jansen

Journal of Near-Death Studies March 1, 1997 DOI: 10.1023/a:1025055109480 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Theoretical or philosophical paper Peer reviewed
Topics Esketamine Ketamine Near-death experience
Key points Proposes that conditions precipitating NDEs may trigger neuroprotective agents that bind to NMDA receptors, producing an altered state of consciousness similar to that induced by ketamine.

Abstract

Near-death experiences (NDEs) can be reproduced by ketamine via blockade of receptors in the brain for the neurotransmitter glutamate, the N-methyl-D-aspartate (NMDA) receptors. Conditions that precipitate NDEs, such as hypoxia, ischemia, hypoglycemia, and temporal lobe epilepsy, have been shown to release a flood of glutamate, overactivating NMDA receptors and resulting in neurotoxicity. Ketamine prevents this neurotoxicity. There are substances in the brain that bind to the same receptor site as ketamine. Conditions that trigger a glutamate flood may also trigger a flood of neuroprotective agents that bind to NMDA receptors to protect cells, leading to an altered state of consciousness like that produced by ketamine.