Background: Neurodegeneration due to neurotoxicity is one of the phenomena in temporal lobe epilepsy. Experimentally, hippocampal excitotoxicity process can occur due to kainic acid exposure, especially in the CA3 area. Neuronal death, astrocyte reactivity and increased calcium also occur in hippocampal excitotoxicity, but few studies have investigated immediate effect after kainic acid exposure. The organotypic hippocampal slice culture (OHSC) is a useful model for studying the neurodegeneration process, but there are still many protocol differences. In this study, minor modifications were made in the OHSC protocol.
Methods: OHSC was obtained from three healthy wild type Wistar rats aged P10. Healthy culture slices were obtained and lasted up to 10 days (DIV 10). Bath application of kainic acid for 48 hours in DIV 10 followed by observation of its initial effects on neurons, astrocytes, and calcium via the expression of MAP2, GFAP, and intracellular calcium imaging, subsequently.
Results: After 48 h of kainic acid administration, there was a significant increase in intracellular calcium intensity (p = 0.006 < α), accompanied by a significant decrease in MAP2 (p = 0.003 < α) and GFAP (p = 0.010 < α) expression.
Conclusion: These findings suggest early neuronal and astrocyte damage at the initial onset of hippocampal injury. This implies that astrocyte damage occurs early before an increase in GFAP that characterizes reactive astrogliosis found in other studies. Damage to neurons and astrocytes may be associated with increased intracellular calcium. It is necessary to develop further research regarding regulation of calcium, MAP2, and GFAP at a spatial time after exposure to kainic acid and strategies to reduce damage caused by excitotoxicity.
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http://dx.doi.org/10.12688/f1000research.126732.3 | DOI Listing |
F1000Res
January 2025
Faculty of Teaching and Education Sciences, Islamic University of Malang, Malang, East Java, Indonesia.
Background: Neurodegeneration due to neurotoxicity is one of the phenomena in temporal lobe epilepsy. Experimentally, hippocampal excitotoxicity process can occur due to kainic acid exposure, especially in the CA3 area. Neuronal death, astrocyte reactivity and increased calcium also occur in hippocampal excitotoxicity, but few studies have investigated immediate effect after kainic acid exposure.
View Article and Find Full Text PDFiScience
January 2025
School of Biosystems and Biomedical Sciences, College of Health Sciences, Korea University, Seoul 02841, Republic of Korea.
TWIK-1 belongs to the two-pore domain K (K2P) channel family, which plays an essential role in the background K conductance of cells. Despite the development of exon 2-deleted knockout (KO) mice, the physiological role of TWIK-1 has remained largely unknown. Here, we observed that the exon 2-deleted KO mice expressed an internally deleted TWIK-1 (TWIK-1 ΔEx2) protein, which unexpectedly acts as a functional K channel.
View Article and Find Full Text PDFActa Pharmacol Sin
January 2025
Department of Anatomy and Convergence Medical Science, College of Medicine, Institute of Medical Science, Tyrosine Peptide Multiuse Research Group, Anti-aging Bio Cell Factory Regional Leading Research Center, Gyeongsang National University, Jinju, Gyeongnam, Republic of Korea.
Glutamine synthetase (GS) plays a crucial role in the homeostasis of the glutamate-glutamine cycle in the brain. Hypoactive GS causes depressive behaviors. Under chronic stress, GS has no change in expression, but its activity is decreased due to nitration of tyrosine (Tyr).
View Article and Find Full Text PDFNeurochem Res
January 2025
Huazhong University of Science and Technology, Tongji Medical College, Wuhan, Hubei, 430000, China.
Epilepsy (EP) is a neurological disorder characterized by abnormal, sudden neuronal discharges. Seizures increase extracellular glutamate levels, causing excitotoxic damage. Glutamate transporter type 1 (GLT-1) and its human homologue excitatory amino acid transporter-2 (EAAT2) clear 95% of extracellular glutamate.
View Article and Find Full Text PDFMol Imaging Biol
January 2025
Paul C. Lauterbur Research Center for Biomedical Imaging, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, Guangdong, China.
Purpose: Proton exchange rate (K) is a valuable biophysical metric. K MRI may augment conventional structural MRI by revealing brain impairments at the molecular level. This study aimed to investigate the feasibility of K MRI in evaluating brain injuries at multiple epilepsy stages.
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