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Author Notes:

Corresponding Author: David Weinshenker, Department of Human Genetics, Emory University School of Medicine, Whitehead 301, 615 Michael St., Atlanta, GA 30322. Phone: (404) 727-3106, Fax: (404) 727-3949, dweinshenker@genetics.emory.edu

We thank C. Strauss for helpful editing of the manuscript.

Subjects:

Research Funding:

SAE was supported by an Epilepsy Foundation Fred Annegers Fellowship (121961), a NINDS Ruth L. Kirschstein National Research Service Award Predoctoral Fellowship (1F31NS065663-01), and a NIDA T32 Institutional Training Grant (DA015040).

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Pharmacology & Pharmacy
  • Epilepsy
  • Depression
  • Animal model
  • Comorbidity
  • DOPAMINE-BETA-HYDROXYLASE
  • GENETIC ABSENCE EPILEPSY
  • TEMPORAL-LOBE EPILEPSY
  • SPIKE-WAVE DISCHARGES
  • RETICULAR THALAMIC NUCLEUS
  • INDUCED STATUS EPILEPTICUS
  • VAGUS NERVE-STIMULATION
  • PRONE RATS
  • BEHAVIORAL ALTERATIONS
  • ANTIEPILEPTIC DRUGS

Rhythm and blues: Animal models of epilepsy and depression comorbidity

Tools:

Journal Title:

Biochemical Pharmacology

Volume:

Volume 85, Number 2

Publisher:

, Pages 135-146

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Clinical evidence shows a strong, bidirectional comorbidity between depression and epilepsy that is associated with decreased quality of life and responsivity to pharmacotherapies. At present, the neurobiological underpinnings of this comorbidity remain hazy. To complicate matters, anticonvulsant drugs can cause mood disturbances, while antidepressant drugs can lower seizure threshold, making it difficult to treat patients suffering from both depression and epilepsy. Animal models have been created to untangle the mechanisms behind the relationship between these disorders and to serve as screening tools for new therapies targeted to treat both simultaneously. These animal models are based on chemical interventions (e.g. pentylenetetrazol, kainic acid, pilocarpine), electrical stimulations (e.g. kindling, electroshock), and genetic/selective breeding paradigms (e.g. genetically epilepsy-prone rats (GEPRs), genetic absence epilepsy rat from Strasbourg (GAERS), WAG/Rij rats, swim lo-active rats (SwLo)). Studies on these animal models point to some potential mechanisms that could explain epilepsy and depression comorbidity, such as various components of the dopaminergic, noradrenergic, serotonergic, and GABAergic systems, as well as key brain regions, like the amygdala and hippocampus. These models have also been used to screen possible therapies. The purpose of the present review is to highlight the importance of animal models in research on comorbid epilepsy and depression and to explore the contributions of these models to our understanding of the mechanisms and potential treatments for these disorders.

Copyright information:

© 2012 Elsevier Inc.

This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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