Title:Decreased Expression of Sox-1 in Cerebellum of Rat with Generalized Seizures Induced by Kindling Model
Volume: 15
Issue: 6
Author(s): Carmen Rubio-Osornio, Aldo Eguiluz-Meléndez, Cristina Trejo-Solís, Veronica Custodio, Moises Rubio-Osornio, Artemio Rosiles-Abonce, Juan C. Martínez-Lazcano, Edith González and Carlos Paz
Affiliation:
Keywords:
Bergmann glia, Cerebellum, Epilepsy, Kindling, Sox-1.
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.
