Background: Epilepsy is one of the most common neurological disorders in humans, and
the role of the cerebellum in its physiopathology remains the subject of study. The Purkinje cells (PC),
whose axons target the dentate and interpositus nuclei, form the main cerebellar output to forebrain
structures involved in epilepsy. Cerebellar atrophy related to loss of PC has been reported in chronic
epilepsy although its mechanism remains unclear. Taking into account that an overexpression of
β-Catenin has been related with cell death, here we present the signaling of β-Catenin and the type of
PC death in cerebellum of rats with seizures induced by the amygdaloid kindling model.
Method: Using an immunohistochemistry and western blot assay for β-Catenin, c-Myc, cyclin D3,
TUNEL and caspase-3, in rats chronically implanted with electrodes, receiving 0, 3, 15, and 45 electrical
Results: We found that such rats suffering a major number of stimuli showed the highest amount of
Conclusion: We concluded that there is a higher activity of the Wnt/β-Catenin pathway associated with
increased number of stimuli may be related with the presence of apoptosis in the cerebellum treated
with amygdala kindling. In this way, we suggest this pathway as one of the mechanisms by which
cerebellar neurons death in generalized seizures.