Do certain signal transduction mechanisms explain the comorbidity of epilepsy and mood disorders?

Epilepsy Behav. 2014 Sep:38:25-31. doi: 10.1016/j.yebeh.2014.01.001. Epub 2014 Jan 25.

Abstract

It is well known that mood disorders are highly prevalent in patients with epilepsy. Although several studies have aimed to characterize alterations in different types of receptors associated with both disturbances, there is a lack of studies focused on identifying the causes of this comorbidity. Here, we described some changes at the biochemical level involving serotonin, dopamine, and γ-aminobutyric acid (GABA) receptors as well as signal transduction mechanisms that may explain the coexistence of both epilepsy and mood disorders. Finally, the identification of common pathophysiological mechanisms associated with receptor-receptor interaction (heterodimers) could allow designing new strategies for treatment of patients with epilepsy and comorbid mood disorders.

Keywords: Anxiety; Depression; G protein; Heterodimers; Homodimers; Receptors; Second messengers; Temporal lobe epilepsy.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Comorbidity*
  • Epilepsy / epidemiology
  • Epilepsy / metabolism*
  • Humans
  • Mood Disorders / epidemiology
  • Mood Disorders / metabolism*
  • Signal Transduction / physiology*