Subanesthetic ketamine reverses neuronal and astroglial metabolic activity deficits in a social defeat model of depression
Open accessAbstract
Depression is one of the most debilitating neuropsychiatric disorders. Most of the current antidepressants have long remission time and low recovery rate. This study explores the impact of ketamine on neuronal and astroglial metabolic activity in prefrontal cortex in a social defeat (SD) model of depression. C57BL/6 mice were subjected to a social defeat paradigm for 5 min a day for 10 consecutive days. Ketamine (10 mg/kg, intraperitoneal) was administered to mice for two consecutive days following the last defeat stress. Mice were infused with [1,6‐13 C 2]glucose or [2‐13 C]acetate to assess neuronal and astroglial metabolic activity, respectively, together with proton‐observed carbon‐edited nuclear magnetic resonance spectroscopy in prefrontal cortex tissue extract. The 13 C labeling of amino acids from glucose and acetate was decreased in SD mice. Ketamine treatment in SD mice restored sucrose preference, social interaction and immobility time to control values. Acute subanesthetic ketamine restored the 13 C labeling of brain amino acids from glucose as well as acetate in SD mice to the respective control values, suggesting that rates of neuronal and astroglial tricarboxylic acid (TCA) cycle and neurotransmitter cycling were re‐established to normal levels. The finding of improved energy metabolism in SD mice suggests that fast anti‐depressant action of ketamine is linked with improved neurotransmitter cycling. image
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In a mouse social defeat model of depression, ketamine restored deficits in markers of neuronal and astroglial metabolic activity in the PFC to normal levels.
“Furthermore, in a mouse social defeat model of depression, ketamine restored deficits in markers of neuronal and astroglial metabolic activity in the PFC to normal levels.111”
From Ketamine as an antidepressant: Overview of its mechanisms of action and potential predictive biomarkers (2020) · cites this paper as [111]
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Matveychuk, D., Thomas, R. K., Swainson, J., Khullar, A., MacKay, M.-A., Baker, G. B., & Dursun, S. M. (2020) · Therapeutic Advances in Psychopharmacology · doi:10.1177/2045125320916657 · Cited by 209 · see citing works
The metabotropic glutamate receptor 5 as a biomarker for psychiatric disorders
(2023) · International Review of Neurobiology · doi:10.1016/bs.irn.2022.10.007 · Cited by 8 · see citing works
- Authors
- Mishra, P. K., Kumar, A., Behar, K. L., & Patel, A. B.
- Affiliations
- Centre for Cellular and Molecular Biology (IN)
- Yale University (US)
- Corresponding author
- Patel, Anant B.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2018-08-16
- Volume
- 146
- Issue
- 6
- Pages
- 722-734
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W2811032630
- Cited by
- 39
- References
- 11
- Citations by year
- 2026: 7 · 2025: 4 · 2024: 4 · 2023: 4 · 2022: 5 · 2021: 7 · 2020: 5 · 2019: 3
- FWCI
- 2.42
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Department of Biotechnology (BT/PR4014/MED/30/673/2011, BT/PR4019/MED/30/675/2011)
- Topics
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- ketamine, subanesthetic ketamine, depression, social defeat, prefrontal cortex, neuronal metabolism, TCA cycle, brain energy metabolism, amino acid labeling, antidepressant mechanism, sucrose preference, immobility time
- MeSH terms
- Acetates, Analgesics, Animals, Astrocytes, Carbon Isotopes, Depressive Disorder, Disease Models, Animal, Food Preferences, Glucose, Hierarchy, Social, Interpersonal Relations, Ketamine, Male, Mice, Inbred C57BL, Neurons, Magnetic Resonance Spectroscopy, Stress, Psychological, Sucrose, Sweetening Agents, Swimming, Mice
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