Objective: Temporal lobe epilepsy (TLE) is one of the most common types of epilepsy syndromes in the world. Depression is an important comorbidity of epilepsy, which has been reported in patients with TLE and in different experimental models of epilepsy. However, there is no established consensus on which brain regions are associated with the manifestation of depression in epilepsy. Here, we investigated the alterations in cerebral glucose metabolism and the metabolic network in the pilocarpine-induced rat model of epilepsy and correlated it with depressive behavior during the chronic phase of epilepsy.
Methods: Fluorodeoxyglucose ( F-FDG) was used to investigate the cerebral metabolism, and a cross-correlation matrix was used to examine the metabolic network in chronically epileptic rats using micro-positron emission tomography (microPET) imaging. An experimental model of epilepsy was induced by pilocarpine injection (320 mg/kg, ip). Forced swim test (FST), sucrose preference test (SPT), and eating-related depression test (ERDT) were used to evaluate depression-like behavior.
Results: Our results show an association between epilepsy and depression comorbidity based on changes in both cerebral glucose metabolism and the functional metabolic network. In addition, we have identified a significant correlation between brain glucose hypometabolism and depressive-like behavior in chronically epileptic rats. Furthermore, we found that the epileptic depressed group presents a hypersynchronous brain metabolic network in relation to the epileptic nondepressed group.
Significance: This study revealed relevant alterations in glucose metabolism and the metabolic network among the brain regions of interest for both epilepsy and depression pathologies. Thus it seems that depression in epileptic animals is associated with a more diffuse hypometabolism and altered metabolic network architecture and plays an important role in chronic epilepsy.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1111/epi.14057 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Itaconate restrains acute proinflammatory activation of microglia MG after traumatic brain injury in mice.
Sci Transl Med
March 2025
Clinical Neuroscience Research Center, Department of Neurosurgery and Neurology, Tulane University School of Medicine, New Orleans, LA 70112, USA.
Traumatic brain injury (TBI) rapidly triggers proinflammatory activation of microglia, contributing to secondary brain damage post-TBI. Although the governing role of energy metabolism in shaping the inflammatory phenotype and function of immune cells has been increasingly recognized, the specific alterations in microglial bioenergetics post-TBI remain poorly understood. Itaconate, a metabolite produced by the enzyme aconitate decarboxylase 1 [IRG1; encoded by immune responsive gene 1 ()], is a pivotal metabolic regulator in immune cells, particularly in macrophages.
View Article and Find Full Text PDFRBC-GEM: A genome-scale metabolic model for systems biology of the human red blood cell.
PLoS Comput Biol
March 2025
Department of Bioengineering, University of California San Diego, La Jolla, California, United States of America.
Advancements with cost-effective, high-throughput omics technologies have had a transformative effect on both fundamental and translational research in the medical sciences. These advancements have facilitated a departure from the traditional view of human red blood cells (RBCs) as mere carriers of hemoglobin, devoid of significant biological complexity. Over the past decade, proteomic analyses have identified a growing number of different proteins present within RBCs, enabling systems biology analysis of their physiological functions.
View Article and Find Full Text PDFPKM2 knockout facilitates the activation of the AMPK/KLF4/ACADVL pathway, leading to increased oxidative degradation of fatty acids in TNBC.
Med Oncol
March 2025
School of Basic Medicine, Gannan Medical University, Ganzhou, 341000, Jiangxi, China.
This study unveils PKM2 as a master metabolic coordinator in triple-negative breast cancer (TNBC), governing the glycolysis-lipolysis balance through the AMPK/KLF4/ACADVL axis. We demonstrate stage-specific PKM2 upregulation in TNBC, with CRISPR/Cas9 knockout inducing dual metabolic reprogramming-suppressed glycolysis and activated lipid catabolism. Mechanistically, PKM2 ablation triggers AMPK-dependent nuclear translocation of KLF4, which directly activates ACADVL (mitochondrial β-oxidation rate-limiting enzyme), explaining lipid droplet depletion.
View Article and Find Full Text PDFResponses of cotton growth, physiology, and soil properties to polyethylene microplastics in arid areas.
Environ Geochem Health
March 2025
Institute of Soil Fertilizer and Agricultural Water Saving, Xinjiang Academy of Agricultural Sciences, Urumqi, 830091, People's Republic of China.
Microplastics (MPs), as a global environmental issue, have unclear impacts on agricultural ecosystems. Cotton, as a major agricultural crop in Xinjiang, requires plastic film covering to ensure its yield. The widespread use of plastic film (commonly made of polyethylene) in cotton cultivation has led to significant concerns about microplastic pollution in cotton fields.
View Article and Find Full Text PDFImpacts of Naphthenic Acids (NAs) Exposure on Soil Bacterial Community and Antibiotic Resistance Genes (ARGs) Dissemination.
Curr Microbiol
March 2025
Key Laboratory of Plant Biotechnology of Liaoning Province, School of Life Sciences, Liaoning Normal University, Dalian, 116081, China.
Naphthenic acids (NAs) are indigenous and complex components in petroleum. In the context of increasing global energy demand, the increasing extraction of fossil resources leads to increased environmental release of NAs, resulting in various environmental risks. However, the impact of NAs exposure on soil microorganisms remains still unclear.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!