Examining the Link between Depression and Epilepsy

Epilepsy News From: Tuesday, September 29, 2015

What was the question the scientists addressed?

Many years of clinical stories and research show that people with epilepsy are approximately 5 times more likely to develop depression. Given the many lifestyle changes and social stressors that often accompany a diagnosis of epilepsy, this may not be a surprising finding. But, did you know that people diagnosed with depression are also at an increased risk of developing epilepsy? Why might this be?

There are numerous possibilities to explain this link. Differences in levels of brain chemicals (called neurotransmitters), alterations in certain brain regions, or hereditary factors in a person’s genes could all play a role. Unfortunately, it is frequently very difficult, if not impossible, to conduct these studies in people. Studying the associations among these potential factors, epilepsy, and depression requires a high level of experimental control over factors like diet, exercise, genetics, and living environment. Also, because people typically have a long life span, it is simply not feasible to conduct many of these studies using human volunteers.

So what can we do? Scientists have long sought to understand this association through the use of animal models, like rats and mice, that can help examine each of these factors in careful, controlled studies. Many aspects of brain anatomy are similar between people and these animal models, and scientists are careful to follow high standards of care to make sure that their animals feel minimal pain and discomfort. For many years, scientists have focused on using animal models of epilepsy to understand the occurrence of depression.

But what about animal models of depression? Do they also develop symptoms of epilepsy? Scientists at Emory University asked this question by studying a unique, animal model of depression to see if the animals would also develop epilepsy, thereby creating the first animal model of depression-associated epilepsy.

What did the scientists do?

The scientists used multiple methods to test for seizure susceptibility and epilepsy-related behaviors in “depression-susceptible” and “depression-resistant” rats. By administering drugs called chemoconvulsants to the rats, the scientists were able to determine if the “depression-susceptible” rats were also more susceptible to seizures, and if they were more likely to develop spontaneous seizures in a process known as epileptogenesis.

The scientists also used an epilepsy model called “kindling” to record EEGs from various brain regions during a mild, painless stimulation that induced a seizure in the rat. This helped the scientists better understand which brain regions were contributing to the seizure behaviors.

What did the scientists learn?

The scientists found that the “depression-susceptible” rats were much more susceptible to chemoconvulsant-induced seizures than the “depression-resistant” rats and that they were also more prone to develop spontaneous seizures several weeks later. This suggests that the “depression-susceptible” rats are also more susceptible to both seizures and epilepsy, similar to clinical findings that show people with depression are also more likely to develop seizures and epilepsy.

The scientists also found that two of the brain regions studied, the amygdala and the hippocampus, are both involved in seizure generation in the “depression-susceptible” rats, with the hippocampus playing an especially important role.

What does this mean?

These findings, along with others from the same labs, suggest that these rats are a useful model of depression-associated epilepsy, the first of its kind. These rats can provide a new tool for scientists to study the causes and treatments for depression and epilepsy occurring in the same individual, and can hopefully provide an important first step in the pathway to improving patient care and quality of life.

Based on work completed in the labs of David Weinshenker & Jay Weiss, Emory University, and as published in Epps et al 2012 

Authored by

Alisha Epps PhD

Reviewed by

Sloka Iyengar PhD

Reviewed Date

Tuesday, September 29, 2015

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