Volume 14, Issue 5 (September & October 2023)                   BCN 2023, 14(5): 663-674 | Back to browse issues page

XML Print

Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:

Rafiei S, Khodagholi F, Gholami Pourbadie H, Dargahi L, Motamedi F. Hepatic Acyl CoA Oxidase1 Inhibition Modifies Brain Lipids and Electrical Properties of Dentate Gyrus. BCN 2023; 14 (5) :663-674
URL: http://bcn.iums.ac.ir/article-1-2194-en.html
1- Neuroscience Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
2- Neurobiology Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
3- Department of Physiology and Pharmacology, Pasteur Institute of Iran, Tehran, Iran.
Introduction: Peroxisomes are essential organelles in lipid metabolism. They contain enzymes for β-oxidation of very long-chain fatty acids (VLCFA) that cannot be broken down in mitochondria. Reduced expression in hepatic acyl-CoA oxidase 1 (ACOX1), a peroxisome β-oxidation enzyme, followed by modification of the brain fatty acid profile has been observed in aged rodents. These studies have suggested a potential role for peroxisome β-oxidation in brain aging. This study was designed to examine the effect of hepatic ACOX1 inhibition on brain fatty acid composition and neuronal cell activities of young rats (200-250 g). 
Methods: A specific ACOX1 inhibitor, 10, 12- tricosadiynoic acid (TDYA), 100 μg/kg (in olive oil) was administered by daily gavage for 25 days in male Wistar rats. The brain fatty acid composition and electrophysiological properties of dentate gyrus granule cells were determined using gas chromatography and whole-cell patch-clamp, respectively. 
Results: A significant increase in C20, C22, C18:1, C20:1, and a decrease of C18, C24, C20:3n6, and C22:6n3 were found in 10, 12- tricosadiynoic acid (TDYA) treated rats compared to the control group. The results showed that ACOX1 inhibition changes fatty acid composition similar to old rats. ACOX1 inhibition caused hyperpolarization of resting membrane potential, and also reduction of input resistance, action potential duration, and spike firing. Moreover, ACOX1 inhibition increased rheobase current and afterhyperpolarization amplitude in granule cells. 
Conclusion: The results indicated that systemic inhibition of ACOX1 causes hypo-excitability of neuronal cells. These results provide new evidence on the involvement of peroxisome function and hepatic ACOX1 activity in brain fatty acid profile and the electrophysiological properties of dentate gyrus cells.
Type of Study: Original | Subject: Cellular and molecular Neuroscience
Received: 2021/06/20 | Accepted: 2023/06/27 | Published: 2023/09/1

Add your comments about this article : Your username or Email:

Send email to the article author

Rights and permissions
Creative Commons License This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

© 2024 CC BY-NC 4.0 | Basic and Clinical Neuroscience

Designed & Developed by : Yektaweb