Objective: This study aimed to determine whether pentylenetetrazol-induced status epilepticus (SE) can induce dentate granule cell neurogenesis in the developing rat and the effect of MK-801, a noncompetitive antagonism of N-methyl-D-aspartate receptor (NMDAR), on neurogenesis.
Methods: Two hundred and sixteen postnatal days 7, 14, 21 or 28 Sprague Dawley (SD) rats were involved in this study. Each age group consisted of 54 rats which were randomly assigned into a SE group, a SE + MK-801 group and a Normal control group (n=18 each). SE was induced by intraperitoneal injection of PTZ (80 mg/kg). The SE + MK-801 group was injected intraperitoneally with MK-801 (1 mg/kg) at 1 hr after SE episode. All rats were given 5-bromodeoxyuridene (BrdU) intraperitonealy to label newborn cells at 6, 13 and 27 days after seizures and then were sacrificed 24 hrs after BrdU injection. The immunohistochemistry method was used to measure the expression of BrdU, TuJl (betaIII tubulin), and glial fibrillary acidic protein (GFAP) in the dentate gyrus of hippocampus of rats.
Results: The number of the BrdU positive cells in the SE group was significantly higher than in the age-matched normal controls at 7 and 14 days after SE episode (P <0.05 or 0.01). Approximately 82.5% and 80.3% of BrdU-labeled cells in the SE and the Control groups were co-expressed TuJ1 respectively. MK-801 treatment decreased the BrdU positive cells compared with the SE group at 7 and 14 days after SE seizures (P < 0.01). On the 28th day after SE episode there were no differences among the three groups for the BrdU positive cells.
Conclusions: PTZ-induced SE can increase the dentate granule cell neurogenesis in the developing rat. NMDAR plays an important role in neurogenesis following seizures.
Download full-text PDF |
Source |
---|
Seizure
January 2025
Department of Neurology, West China Hospital of Sichuan University, Chengdu, Sichuan Province, PR China; Institute of Brain Science and Brain-Inspired Technology of West China Hospital, Sichuan University, Chengdu, Sichuan Province, PR China. Electronic address:
Background: The etiology of status epilepticus (SE) in Tibet has not yet been reported. We aimed to establish the etiological baseline of SE in the Tibet Autonomous Region in China and compare it with a SE cohort from a regional neuroscience centre in Sichuan, Southwestern China to reveal whether there was a unique etiology distribution in the Tibetan region.
Methods: We retrospectively captured clinical data of patients diagnosed with SE in the People's Hospital of Xizang Autonomous Region from January 2015 to December 2020.
Life (Basel)
January 2025
Neurology Service, Faculty of Veterinary Medicine, "Ion Ionescu de la Brad" Iași University of Life Sciences, 700489 Iași, Romania.
Hepatic encephalopathy (HE) in dogs is a metabolic disorder of the central nervous system that occurs secondarily to liver dysfunctions, whether due to acquired or congenital causes. A portosystemic shunt is the presence of abnormal communications between the hepatic vessels (portal and suprahepatic veins). As a result of this, the blood brought from the digestive tract through the portal vein bypasses the liver, and the unmetabolized components of the portal bloodstream enter directly into systemic circulation, causing clinical symptoms of metabolic encephalopathy (HE).
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Institute for Maternal and Child Health IRCCS Burlo Garofolo, Via dell'Istria, 65, 34137 Trieste, Italy.
Pathogenic variants in , encoding dynamin-like protein-1 (DRP1), cause a lethal encephalopathy. DRP1 defective function results in altered mitochondrial networks, characterized by elongated/spaghetti-like, highly interconnected mitochondria. We validated in yeast the pathogenicity of a de novo variant identified by whole exome sequencing performed more than 10 years after the patient's death.
View Article and Find Full Text PDFBiomolecules
January 2025
Department of Neurology, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
Reactive astrogliosis and acidosis, common features of epileptogenic lesions, express a high level of astrocytic acid-sensing ion channel-1a (ASIC1a), a proton-gated cation channel and key mediator of responses to neuronal injury. This study investigates the role of astrocytic ASIC1a in cognitive impairment following epilepsy. Status epilepticus (SE) in C57/BL6 mice was induced using lithium-pilocarpine; the impact of ASIC1a on astrocytes was assessed using rAAV-ASIC1a-NC and rAAV-ASIC1a-shRNA, injected in the CA3 region of mice.
View Article and Find Full Text PDFChildren (Basel)
December 2024
Department of Oncology and Hematology, Children's Hospital Zagreb, Klaićeva 16, 10000 Zagreb, Croatia.
: Recent advances in childhood acute lymphoblastic leukemia (ALL) and lymphoblastic lymphoma (LL) management provide higher survival rates at the cost of increased toxicities. Acute neurotoxicity affects up to 10% of patients, requiring rapid recognition and treatment. : A retrospective observational study was performed to determine the frequency, clinical manifestations, radiological characteristics, treatment options and outcome of acute neurological adverse events in pediatric patients with lymphoid malignancies at the Department of Oncology and Hematology, Children's Hospital Zagreb, Croatia.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!