Aim: This study aimed to assess the changes in neuronal density in CA1 and CA3 regions in the hippocampus of young adulthood and middle age rat model after feeding by ethanolic extract.
Materials And Methods: In this research, 30 male Wistar rats consist of young to middle-aged rats were divided into three groups (3, 6, and 9 months old) and treated with a different dosage of ethanolic extract (0, 50, and 100 mg/kg b.w.) for 45 days. Furthermore, cresyl violet staining was performed to analyze hippocampus formation mainly in CA1 and CA3 area. The concentrations of acetylcholine (Ach) in brain tissues were analyzed by enzyme-linked immunosorbent assay.
Results: In our models using rat model, we found that the administration of ethanolic extract with a dosage of 100 mg/kg b.w. for 45 days induced the density of pyramidal cells significantly in CA1 and CA3 of the hippocampus. These results were supported by an increase of Ach concentrations on the brain tissue.
Conclusions: The administration of ethanolic extract may promote the density of the pyramidal cells in the CA1 and CA3 mediated by the up-regulated concentration of Ach.
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http://dx.doi.org/10.14202/vetworld.2018.135-140 | DOI Listing |
Previously, our metabolomic, transcriptomic, and genomic studies characterized the ceramide/sphingomyelin pathway as a therapeutic target in Alzheimer's disease, and we demonstrated that FTY720, a sphingosine-1-phospahate receptor modulator approved for treatment of multiple sclerosis, recovers synaptic plasticity and memory in APP/PS1 mice. To further investigate how FTY720 rescues the pathology, we performed metabolomic analysis in brain, plasma, and liver of trained APP/PS1 and wild-type mice. APP/PS1 mice showed area-specific brain disturbances in polyamines, phospholipids, and sphingolipids.
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Department of Physiology, School of Medicine, University College Cork, Western Road, Cork, Ireland.
Duchenne muscular dystrophy (DMD), an X-linked neuromuscular disorder, characterised by progressive immobility, chronic inflammation and premature death, is caused by the loss of the mechano-transducing signalling molecule, dystrophin. In non-contracting cells, such as neurons, dystrophin is likely to have a functional role in synaptic plasticity, anchoring post-synaptic receptors. Dystrophin-expressing hippocampal neurons are key to cognitive functions such as emotions, learning and the consolidation of memories.
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Biochemistry and Molecular Biology Laboratory, Department of Zoology, Institute of Science, Banaras Hindu University, Varanasi, 221 005, India.
Hypoxia is a significant stressor, and stabilized hypoxia-inducible factor-1α (HIF-1α) regulates the expression of numerous genes, leading to various biochemical, molecular, physiological and genomic changes. The body's oxygen-sensing system activates gene expression to protect brain tissues from hypoxia. Gamma-aminobutyric acid, an inhibitory neurotransmitter, regulates brain excitability during hypoxia through the activation of HIF-1 α.
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Department of Pharmacology "Otto Orsingher", Institute of Experimental Pharmacology of Córdoba (IFEC-CONICET), Faculty of Chemical Sciences, National University of Córdoba, X5000 Córdoba, Argentina.
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View Article and Find Full Text PDFFront Comput Neurosci
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Center for Synaptic Brain Dysfunctions, Institute for Basic Science, Daejeon, Republic of Korea.
Memory consolidation refers to the process of converting temporary memories into long-lasting ones. It is widely accepted that new experiences are initially stored in the hippocampus as rapid associative memories, which then undergo a consolidation process to establish more permanent traces in other regions of the brain. Over the past two decades, studies in humans and animals have demonstrated that the hippocampus is crucial not only for memory but also for imagination and future planning, with the CA3 region playing a pivotal role in generating novel activity patterns.
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