Use Of Rapid Amygdala Kindling With Corticosterone Supplementation As A Model Of Epilepsy-Depression Comorbidity

Description

Temporal lobe epilepsy increases risk for developing major depression, and conversely, depression increases risk for development of epilepsy. The mechanisms responsible for the widely observed bi-directional relationship between epilepsy and depression are currently poorly understood. One reason why our understanding of shared etiology has had little improvement is due to the lack of availability of a reliable animal model for inducing depression in epileptic animals. The development of a reliable model of epilepsy-depression comorbidity would greatly improve the ability to mechanistically evaluate shared pathophysiology between the conditions. Recently there has been evidence that rapid kindling of the basolateral amygdala can evoke a behavioural phenotype that is comparable to the symptoms of anxiety and depression observed in depressed epileptic patients. However, this work has yet to be replicated, leaving question as to whether or not the behavioural phenotype can be reliably evoked. In the following series of experiments we assessed rapid amygdala kindling as a potential model of epilepsy-depression comorbidity and sought to improve the model with inclusion of the glucocorticoid corticosterone. Our findings may improve our understanding of the unique relationships between epilepsy and depression.
Author Keywords: animal models, depression, hippocampus, kindling, stress, temporal lobe epilepsy