Background: Experimental complex febrile seizures induce a persistent hippocampal hyperexcitability and an enhanced seizure susceptibility in adulthood. The rearrangement of filamentous actin (F-actin) enhances the excitability of hippocampus and contributes to epileptogenesis in epileptic models. However, the remodeling of F-actin after prolonged febrile seizures is to be determined.
Methods: Prolonged experimental febrile seizures were induced by hyperthermia on P10 and P14 rat pups. Changes of actin cytoskeleton in hippocampal subregions were examined at P60 and the neuronal cells and pre- /postsynaptic components were labeled.
Results: F-actin was increased significantly in the stratum lucidum of CA3 region in both HT + 10D and HT + 14D groups and further comparison between the two groups showed no significant difference. The abundance of ZNT3, the presynaptic marker of mossy fiber (MF)-CA3 synapses, increased significantly whereas the postsynaptic marker PSD95 did not change significantly. Overlapping area of F-actin and ZNT3 showed a significant increase in both HT+ groups. The results of cell counts showed no significant increase or decrease in the number of neurons in each area of hippocampus.
Conclusion: F-actin was significantly up-regulated in the stratum lucidum of CA3, corresponding to the increase of the presynaptic marker of MF-CA3 synapses after prolonged febrile seizures, which may enhance the excitatory output from the dentate gyrus to CA3 and contribute to the hippocampal hyperexcitability.
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http://dx.doi.org/10.3389/fneur.2023.1107538 | DOI Listing |
Pediatr Infect Dis J
January 2025
From the Department of Pediatrics, Niigata University, Graduate School of Medical and Dental Sciences, Niigata, Japan.
Background: The spread of the BA.5 Omicron variant of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has increased the number of hospitalized children. However, the impact of the spread of new omicron subvariants in children remains poorly described.
View Article and Find Full Text PDFAm J Med Genet B Neuropsychiatr Genet
January 2025
Department of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, the Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
The RYR3 gene encodes a brain-type ryanodine receptor that functions to release calcium from intracellular storage and plays an essential role in calcium signaling. The associations between RYR3 variants and brain disorders remain unknown. We performed whole-exome sequencing in patients with idiopathic (non-lesional) partial epilepsy of unknown etiology.
View Article and Find Full Text PDFAnn Clin Transl Neurol
January 2025
Department of Pharmacology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.
Objective: Interpretation of clinical genetic testing, which identifies a potential genetic etiology in 25% of children with epilepsy, is limited by variants of uncertain significance. Understanding functional consequences of variants can help distinguish pathogenic from benign alleles. We combined automated patch clamp recording with neurophysiological simulations to discern genotype-function-phenotype correlations in a real-world cohort of children with SCN1A-associated epilepsy.
View Article and Find Full Text PDFFront Syst Neurosci
January 2025
Neurology Unit, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
Introduction: Evidence increasingly shows that facial emotion recognition (FER) is impaired in refractory mesial temporal lobe epilepsy (rMTLE), especially in patients with a right focus. This study explores FER in both mild (mMTLE) and refractory forms, examining the influence of epileptic focus lateralization on FER.
Methods: 50 MTLE patients, categorized by epilepsy severity and focus lateralization, were compared with healthy controls.
Gene
January 2025
Department of Neurology Children's Hospital of Chongqing Medical University, China; National Clinical Research Center for Child Health and Disorders, China; Ministry of Education Key Laboratory of Child Development and Disorders, China; Chongqing Key Laboratory of Child Neurodevelopment and Cognitive Disorders, China. Electronic address:
Mutations in ADGRV1 can cause seizures, but the mechanism remains unclear. The zebrafish model can be used to assess the functions of human ADGRV1 and its variant alleles during embryonic development. In this study, we summarized the phenotypic and genotypic characteristics of four children with ADGRV1 variation and based on this, we validated the ADGRV1 loss phenotype in an adgrv1-knockout zebrafish model.
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