title: Decreased Expression of Sox-1 in Cerebellum of Rat with Generalized Seizures Induced by Kindling Model.
abstract: The single feature of all malformations in cortical development is the clinical association with epilepsy. It has been proven that Sox-1 expression is essential during neurodevelopment and it is reported that Sox-1 knockout mice present spontaneous generalized seizures. Particularly in cerebellum, Sox-1 plays a key role in the Bergmann´s glia (BG) function, which allows the correct function of the Purkinje cells (PC). The targets of PC are the dentate and interpositus nuclei, which form the main cerebellar efferents involved in the physiopathology of epilepsy. Here we present the Sox-1 expression in cerebellum of rats during electric amygdala-kindling. We obtained seizures and once they had 3, 15 and 45 electric stimuli, the animals were sacrificed; the cerebellum was processed for inmunohistochemistry and Western blot analysis was performed to determine Sox-1 expression. Liquid chromatography was performed to examine gammaaminobutyric acid (GABA) and glutamate concentration. According to the literature, a progressive increase was observed in the electrographic and behavioral parameters. We found that Sox-1 expression in 15 and 45-stimuli groups had a statistically significant decrease as compared with controls, while the 3-stimuli group was similar to the control group. The concentration of glutamate was increased in rats with 45 stimuli. We can conclude that Sox-1 expression decreases as the number of seizures increases, and this is probably due to an altered glutamate regulation by a dysfunctional BG. In this way, we can suggest this mechanism as a one possible explanation of how the cerebellum participates in the pathophysiology of epilepsy.
authors.forename: Carmen
authors.initials: C
authors.lastname: Rubio-Osornio
authors.forename: Aldo
authors.initials: A
authors.lastname: Eguiluz-Meléndez
authors.forename: Cristina
authors.initials: C
authors.lastname: Trejo-Solís
authors.forename: Veronica
authors.initials: V
authors.lastname: Custodio
authors.forename: Moises
authors.initials: M
authors.lastname: Rubio-Osornio
authors.forename: Artemio
authors.initials: A
authors.lastname: Rosiles-Abonce
authors.forename: Juan C
authors.initials: JC
authors.lastname: Martínez-Lazcano
authors.forename: Edith
authors.initials: E
authors.lastname: González
authors.affiliation: Instituto Nacional de Neurología y Neurocirugía M.V.S. Insurgentes sur 3867 col. La fama 14269, México D.F., México. paztres@unam.mx.
authors.forename: Carlos
authors.initials: C
authors.lastname: Paz
mesh_terms: D000679:Amygdala / Q000378:metabolism / Q000473:pathology; D000818:Animals; D015153:Blotting, Western; D002531:Cerebellum / Q000378:metabolism* / Q000473:pathology; D002851:Chromatography, High Pressure Liquid; D004195:Disease Models, Animal; D018450:Disease Progression; D004558:Electric Stimulation; D004829:Epilepsy, Generalized / Q000378:metabolism* / Q000473:pathology; D018698:Glutamic Acid / Q000378:metabolism; D007150:Immunohistochemistry; D007696:Kindling, Neurologic / Q000378:metabolism / Q000473:pathology; D009457:Neuroglia / Q000378:metabolism / Q000473:pathology; D017208:Rats, Wistar; D064568:S100 Calcium Binding Protein beta Subunit / Q000378:metabolism; D055748:SOXB1 Transcription Factors / Q000378:metabolism*; D012640:Seizures / Q000378:metabolism* / Q000473:pathology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
chemical_list: D064568:S100 Calcium Binding Protein beta Subunit; C579158:S100b protein, rat; D055748:SOXB1 Transcription Factors; C490908:Sox1 protein, rat; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid