PMID- 34566558
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20230908
IS  - 1662-4548 (Print)
IS  - 1662-453X (Electronic)
IS  - 1662-453X (Linking)
VI  - 15
DP  - 2021
TI  - Ketamine: Neuroprotective or Neurotoxic?
PG  - 672526
LID - 10.3389/fnins.2021.672526 [doi]
LID - 672526
AB  - Ketamine, a non-competitive N-methyl-D-aspartate receptor (NMDAR) antagonist, has 
      been employed clinically as an intravenous anesthetic since the 1970s. More 
      recently, ketamine has received attention for its rapid antidepressant effects 
      and is actively being explored as a treatment for a wide range of 
      neuropsychiatric syndromes. In model systems, ketamine appears to display a 
      combination of neurotoxic and neuroprotective properties that are context 
      dependent. At anesthetic doses applied during neurodevelopmental windows, 
      ketamine contributes to inflammation, autophagy, apoptosis, and enhances levels 
      of reactive oxygen species. At the same time, subanesthetic dose ketamine is a 
      powerful activator of multiple parallel neurotrophic signaling cascades with 
      neuroprotective actions that are not always NMDAR-dependent. Here, we summarize 
      results from an array of preclinical studies that highlight a complex landscape 
      of intracellular signaling pathways modulated by ketamine and juxtapose the 
      somewhat contrasting neuroprotective and neurotoxic features of this drug.
CI  - Copyright (c) 2021 Choudhury, Autry, Tolias and Krishnan.
FAU - Choudhury, Divya
AU  - Choudhury D
AD  - Department of BioSciences, Rice University, Houston, TX, United States.
FAU - Autry, Anita E
AU  - Autry AE
AD  - Dominick P. Purpura Department of Neuroscience, Albert Einstein College of 
      Medicine, Bronx, NY, United States.
AD  - Department of Psychiatry and Behavioral Sciences, Albert Einstein College of 
      Medicine, Bronx, NY, United States.
FAU - Tolias, Kimberley F
AU  - Tolias KF
AD  - Department of Neuroscience, Baylor College of Medicine, Houston, TX, United 
      States.
FAU - Krishnan, Vaishnav
AU  - Krishnan V
AD  - Department of Neuroscience, Baylor College of Medicine, Houston, TX, United 
      States.
AD  - Department of Neurology, Baylor College of Medicine, Houston, TX, United States.
AD  - Department of Psychiatry and Behavioral Sciences, Baylor College of Medicine, 
      Houston, TX, United States.
LA  - eng
GR  - P50 HD105352/HD/NICHD NIH HHS/United States
GR  - R01 MH109511/MH/NIMH NIH HHS/United States
GR  - R01 NS062829/NS/NINDS NIH HHS/United States
GR  - RF1 NS062829/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Review
DEP - 20210910
PL  - Switzerland
TA  - Front Neurosci
JT  - Frontiers in neuroscience
JID - 101478481
PMC - PMC8461018
OTO - NOTNLM
OT  - AMPA receptor
OT  - BDNF
OT  - NMDA receptor
OT  - antidepressant
OT  - ketamine mechanism
OT  - ketamine-induced neurotoxicity
OT  - neuroprotection
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2021/09/28 06:00
MHDA- 2021/09/28 06:01
PMCR- 2021/01/01
CRDT- 2021/09/27 06:01
PHST- 2021/02/26 00:00 [received]
PHST- 2021/07/12 00:00 [accepted]
PHST- 2021/09/27 06:01 [entrez]
PHST- 2021/09/28 06:00 [pubmed]
PHST- 2021/09/28 06:01 [medline]
PHST- 2021/01/01 00:00 [pmc-release]
AID - 10.3389/fnins.2021.672526 [doi]
PST - epublish
SO  - Front Neurosci. 2021 Sep 10;15:672526. doi: 10.3389/fnins.2021.672526. 
      eCollection 2021.