Molecular Mechanisms and Toxic Effects of Ketamine.
Level 5 - mechanism / opinion, no new human data
Narrative review of molecular mechanisms and toxicological pathways without systematic methodology or primary empirical data
PubMed 40813080 · doi:10.12116/j.issn.1004-5619.2024.341002
What was done
This narrative review summarized the molecular mechanisms underlying the pharmacological actions and toxic effects of ketamine, focusing on its receptor targets and ion channel interactions to provide a reference for forensic identification of abuse and toxicity phenotypes.
What was found
The abstract reports no quantitative data or numerical outcomes. It describes ketamine's primary mechanism as N-methyl-D-aspartate receptor (NMDAR) blockade, with additional activity across AMPA receptors, opioid receptors, GABA receptors, monoaminergic receptors, cholinergic receptors, hyperpolarization-activated cyclic nucleotide-gated (HCN) channels, voltage-gated sodium channels, and L-type voltage-dependent calcium channels. Toxic side effects noted include nerve damage, psychological dependence, and adverse emotional reactions.
Why it matters
The review provides a broad molecular overview intended to help forensic specialists recognize clinical and post-mortem toxicity phenotypes associated with ketamine abuse.
Limits
This is an unsystematic narrative review offering no primary human data, quantitative synthesis, or detailed search methodology in the abstract. Specific dose-toxicity thresholds, effect sizes, and study selection criteria are not reported.
Cited by
- supports Ketamine is classified pharmacologically as a dissociative anesthetic.