Regional brain dysregulation of Ca2+-handling systems in ketamine-induced rat model of experimental psychosis
Malwina Lisek, T. Boczek, Bozena Ferenc, L. Zylinska
Cell and tissue research December 21, 2015 DOI: 10.1007/s00441-015-2332-3 (opens in new tab)
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Study at a glance
AI-extracted from the abstract| Characteristics | Animal experimental study Peer reviewed |
|---|---|
| Population | Rats |
| Intervention | Ketamine |
| Topics | Esketamine Ketamine |
| Key findings | Chronic ketamine administration in rats increased intracellular calcium in all brain regions examined, but cytosolic calcium changes correlated with hyperlocomotor activity only in the cortex and striatum. The authors suggest that an imbalance between calcium 'on' and 'off' systems contributes to disrupted calcium homeostasis, and identify ketamine-affected genes as possible etiological factors in schizophrenia. |
Abstract
Chronic N-methyl-D-aspartate receptor (NMDAR) antagonist treatment can provide valuable neurochemical and neuroanatomical models of experimental psychosis. One such antagonist, ketamine, with its short half-time and well-documented psychotomimetic action, has cognitive effects resembling various aspects of schizophrenia-like symptoms. In order to obtain insights into possible relationships between Ca2+ homeostasis and schizophrenia-related symptoms, we investigate the effects of chronic ketamine administration on intracellular Ca2+ levels in various brain regions and on the expression level of key members of the neuronal Ca2+-handling system in rats. We show increased intracellular [Ca2+] in all of the examined brain regions following ketamine treatment but an altered cytosolic Ca2+ level correlated with hyperlocomotor activity was only established for the cortex and striatum. Our findings also suggest that an imbalance in the expression between the calcium “on” and “off” systems contributes to the deregulation of brain Ca2+ homeostasis in our ketamine-induced model of experimental psychosis. Identification of the genes whose expression is affected by ketamine treatment indicates their involvement as putative etiological factors in schizophrenia.
Comparable studies
Other preclinical and animal studies on ketamine, most cited first.
| Study | Year | Design | Participants |
|---|---|---|---|
| mTOR-Dependent Synapse Formation Underlies the Rapid Antidepressant Effects of NMDA Antagonists Rats | 2010 | Observational study | |
| Activation of Glutamatergic Neurotransmission by Ketamine: A Novel Step in the Pathway from NMDA Receptor Blockade to Dopaminergic and Cognitive Disruptions Associated with the Prefrontal Cortex Conscious rats | 1997 | Dose-response study with microdialysis and behavioral testing | |
| NMDAR inhibition-independent antidepressant actions of ketamine metabolites Mice | 2016 | Preclinical study | |
| The dissociative anaesthetics, ketamine and phencyclidine, selectively reduce excitation of central mammalian neurones by N‐methyl‐aspartate Spinal neurons in decerebrate or pentobarbitone-anaesthetized cats and rats | 1983 | Experimental study | |
| R-ketamine: a rapid-onset and sustained antidepressant without psychotomimetic side effects Mice | 2015 | Experimental study |
Citations in the library
Cited by 5
- Ketamine and Ketamine Metabolite Pharmacology: Insights into Therapeutic Mechanisms Pharmacological Reviews June 26, 2018
- Effect of Acute Ketamine Treatment on Sympathetic Regulation Indexed by Electrodermal Activity in Adolescent Major Depression. Pharmaceuticals March 10, 2024
- Gastrodin Mitigates Ketamine-Induced Inhibition of F-Actin Remodeling and Cell Migration by Regulating the Rho Signaling Pathway. Biomedicines March 6, 2025
- Treadmill Exercise Training Ameliorates Apoptotic Cells and DNA Oxidation in the Cerebral Cortex of Rats Exposed to Chronic Ketamine Abuse. Addiction Biology March 1, 2025
- Glutamate Deregulation in Ketamine-Induced Psychosis—A Potential Role of PSD95, NMDA Receptor and PMCA Interaction Frontiers in Cellular Neuroscience June 28, 2017