Do certain signal transduction mechanisms explain the comorbidity of epilepsy and mood disorders?
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.
Department of Pharmacobiology, Center of Research and Advanced Studies, Mexico City, Mexico. Electronic address: lrocha@cinvestav.mx.
Luisa
L
Rocha
National Institute of Neurology and Neurosurgery "Manuel Velasco Suarez", Mexico City, Mexico.
Mario
M
Alonso-Vanegas
Unit for Medical Research in Neurological Diseases, National Medical Center, Mexico City, Mexico.
Sandra
S
Orozco-Suárez
Department of Pharmacobiology, Center of Research and Advanced Studies, Mexico City, Mexico.
David
D
Alcántara-González
University Center of Biomedical Research, University of Colima, Colima, Mexico.
Humberto
H
Cruzblanca
University Center of Biomedical Research, University of Colima, Colima, Mexico.
Elena
E
Castro
D015897:Comorbidity; D004827:Epilepsy / Q000453:epidemiology / Q000378:metabolism*; D006801:Humans; D019964:Mood Disorders / Q000453:epidemiology / Q000378:metabolism*; D015398:Signal Transduction / Q000502:physiology*
Anxiety; Depression; G protein; Heterodimers; Homodimers; Receptors; Second messengers; Temporal lobe epilepsy