The Ketamine Model of the Near-Death Experience: A Central Role for the N-Methyl-D-Aspartate Receptor
Journal of Near-Death Studies March 1, 1997 DOI: 10.1023/a:1025055109480 (opens in new tab) via Semantic Scholar
Summary
AI-generated from the abstractKetamine can reproduce near-death experiences (NDEs) by blocking NMDA receptors for the neurotransmitter glutamate in the brain. Conditions that trigger NDEs—such as hypoxia, ischemia, hypoglycemia, and temporal lobe epilepsy—release a surge of glutamate that overactivates NMDA receptors, causing neurotoxicity. Ketamine prevents this neurotoxicity. The brain contains substances that bind to the same receptor site as ketamine. Conditions causing a glutamate flood may also release neuroprotective agents that bind to NMDA receptors, protecting cells and inducing an altered state of consciousness similar to that produced by ketamine.
Study at a glance
| Characteristics | Theoretical or philosophical paper Peer reviewed |
|---|---|
| Keywords | Psychology Medicine |
| Key finding | 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.