Omega-3 fatty acid reverses Ketamine-induced hyperlocomotion, memory deficit and cerebral cortex neuronal injury in rats
Olakunle Onaolapo, Adejoke Onaolapo
Acta Bioscientia: Journal of Biomedical and Biological Science Research January 25, 2025 DOI: 10.71181/actabioscientia12170 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Randomized controlled trial Peer reviewed |
|---|---|
| Sample size | 50 |
| Population | Rats (130-150g) |
| Interventions | Omega-3 fatty acids Olanzapine |
| Dose | 250 and 500 mg/kg orally for omega-3 fatty acids; 2 mg/kg for olanzapine |
| Duration | 14-day treatment period |
| Measures | open field arena, elevated Plus maze, Y-Maze, malondialdehyde (MDA), Total antioxidant capacity (TAC), interleukin (IL)-6, IL-1β, histological analysis |
| Topics | Esketamine Ketamine |
| Key findings | Omega-3 fatty acids reversed ketamine-induced behavioral changes, oxidative stress, inflammation, and neuronal degeneration in rats. |
Abstract
Schizophrenia (SZ) a chronic debilitating mental disorder affecting approximately 1% of the population globally. While understanding of pathophysiology, neuropathology and treatment have advance significantly; resistance to therapy and treatment failures necessitate the search for novel compounds like omega-3 fatty acids (OMG). This study investigated the effects of OMG on ketamine-induced brain changes in rats. Fifty rats (130-150g) were assigned into five groups (n=10); group A (control) received distilled water intraperitoneally (i.p.), while rats in groups B-E were treated with ketamine (15 mg/kg i.p) for 10 days. Subsequently, rats in groups A and B (Ketamine control) received distilled water orally at 10 ml/kg while C and D received OMG at 250 and 500 mg/kg orally. Rats in group E received olanzapine (standard therapy) at 2 mg/kg, Treatments were for 14 days following which animals were exposed to the open field arena, elevated Plus and Y-Maze. Twenty-four hours after the last test rats were euthanised, and blood was taken for estimation of malondialdehyde (MDA), Total antioxidant capacity (TAC), and interleukin (IL)-6 and -1β. The cerebral cortex was sectioned and processed for histological analysis. Results showed an increase in horizontal locomotion and rearing, memory impairment and increased oxidative stress and proinflammation with ketamine, which was reversed with OMG at 250 and 500 and olanzapine . Cerebral cortex histomorphology revealed presence og neuronal degeneration with ketamine and variable degrees of reversal with OMG and Olanzapine. In conclusion this study demonstrated the possible neuroprotective effects of OMG in mitigating ketamine induced changes in rats. However, more studies would be required to ascertain its benefits in humans
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 |