Ultrastructure of the cerebral and cerebellar cortex, hippocampus and nucleus facialis was examined in albino rats during MSO convulsions. Three, 6 and 12 h after peritoneal injection of the drug (600 mg/kg) perfusion and dissection were done. Convulsions appeared 4-5 h, status epilepticus 8-9 h after drug administration. Following the onset of clinical seizures, the mitochondria of the neurons became severely damaged. The vesicles and cisterns of the Golgi complex and the endoplasmic reticulum dilated considerably. In the synapses the vesicles were packed together, their number gradually decreased. The astroglia became highly oedematous. During status epilepticus, dark cells and a thickening of the synaptic membranes could be seen beside the above alterations. The morphological changes were most prominent in the cerebellar cortex and in the h1 area of the hippocampus. The neuronal structure of the cerebral cortex was the least damaged.
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Neurol Sci
January 2025
Neurology Department One, Dongfang Hospital, Beijing University of Chinese Medicine, No. 6, Fangxingyuan Community, Fangzhuang, Fengtai District, Beijing, 100078, People's Republic of China.
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Behav Brain Res
January 2025
Normandie Univ, UNICAEN, INSERM, PhIND "Physiopathology and Imaging of Neurological Disorders", Cyceron, 14000 Caen, France; Institut Universitaire de France (IUF).
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View Article and Find Full Text PDFInt J Mol Sci
January 2025
Department of Neuroregeneration, Netherlands Institute for Neuroscience, Royal Netherlands Academy of Arts and Sciences, Meibergdreef 47, 1105 BA Amsterdam, The Netherlands.
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View Article and Find Full Text PDFInt J Mol Sci
January 2025
Laboratory of Neuronal Plasticity and Neurorepair, Institute of Neuroscience of Castile and Leon (INCyL), Universidad de Salamanca, 37007 Salamanca, Spain.
In recent decades, the scientific community has faced a major challenge in the search for new therapies that can slow down or alleviate the process of neuronal death that accompanies neurodegenerative diseases. This study aimed to identify an effective therapy using neurotrophic factors to delay the rapid and aggressive cerebellar degeneration experienced by the Purkinje Cell Degeneration (PCD) mouse, a model of childhood-onset neurodegeneration with cerebellar atrophy (CONDCA). Initially, we analyzed the changes in the expression of several neurotrophic factors related to the degenerative process itself, identifying changes in insulin-like growth factor 1 (IGF-1) and Vascular Endothelial Growth Factor B (VEGF-B) in the affected animals.
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