Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2022 Jan 18;12:797577. doi: 10.3389/fpsyt.2021.797577

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

Copyright © 2022 Gagne, Piot and Brake.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

PMC Copyright notice

Ketamine's effects on the kynurenine pathway leads to lowered levels of neurotoxic quinolinic acid (QUIN) via inhibition of cytokine production, and lowered effects of QUIN/NMDA binding by blocking the NMDA receptor. (1) Ketamine binding blocks the NMDA receptor, reducing the neurotoxic effects of QUIN released from microglia. (2) This decreased neurotoxicity decreases ATP release from the synapse. (3) As a result, the microglia no longer extend toward this “find me” signal and the inflammatory reaction is dampened, and the microglia assumes a less reactive state. In addition, ketamine was found to mitigate the reaction of microglia to inflammatory stimuli such as stress or LPS and decreased the production of proinflammatory cytokines. Created with BioRender.com.