Format

Send to

Choose Destination
Chem Biol Interact. 2020 Mar 1;319:109006. doi: 10.1016/j.cbi.2020.109006. Epub 2020 Feb 19.

Ketamine a dissociative anesthetic: Neurobiology and biomolecular exploration in depression.

Author information

1
Department of Anesthesiology, The Second Hospital of Jilin University, Changchun, Jilin, China.
2
Department of Anesthesiology, The Second Hospital of Jilin University, Changchun, Jilin, China. Electronic address: zhao_ppeng@aliyun.com.

Abstract

Ketamine is gaining ground as a potential treating depression because it has a distinct mode of action than typical drugs that influence monoamine neurotransmitters including noradrenaline, dopamine, or serotonin. Ketamine is thought to act by blocking N-methyl-d-aspartate (NMDA) receptors in the brain, which interact with the amino acid neurotransmitter glutamate. The resultant chemical changes in the brain caused by ketamine are not yet fully understood but could involve ketamine-induced gene expression and signaling cascades that act long after the drug has been eliminated from the body. Despite these remarkable effects, the widespread use of ketamine is limited by potential side effects including the emergence reactions (hallucinations, dreams, and out-of-body experiences) by recreational users, who need further study before long-term use of ketamine can be approved for depression. Thus, studies are necessary to further elucidate mechanistic actions of ketamine at cellular and network levels. Thus, we are exploring the involvement of molecular targets for the treatment and psychomimetic phenomena of the ketamine.

KEYWORDS:

Brain-derived neurotrophic factor; Endocannabinoid system; Histone deacetylase 5; Mitogen-activated protein kinase; N-methyl d-Aspartate receptor; Δ(9)-tetrahydrocannabinol

PMID:
32084352
DOI:
10.1016/j.cbi.2020.109006
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center