Laura Colino1, Javier Herranz-Herrer1, Elena Gil-Benito1, Teresa Ponte-Lopez1, Pablo Del Sol-Calderon1, Maria Rodrigo-Yanguas1, María Gil-Ligero2, Antonio J Sánchez-López2,3,4, Jose de Leon5,6,7, Hilario Blasco-Fontecilla8,9,10. 1. Department of Psychiatry, Puerta de Hierro University Hospital-Segovia de Arana Health Research Institute (IDIPHISA), Madrid, Spain. 2. Biobank, Puerta de Hierro University Hospital-IDIPHISA, Madrid, Spain. 3. Neuroimmunology Unit, Puerta de Hierro University Hospital Segovia de Arana Health Research Institute (IDIPHISA), Madrid, Spain. 4. Multiple Sclerosis Spanish Net (REEM), Madrid, Spain. 5. Mental Health Research Center at Eastern State Hospital, Lexington, KY, USA. 6. Psychiatry and Neurosciences Research Group (CTS-549), Institute of Neurosciences, University of Granada, 18971, Granada, Spain. 7. Biomedical Research Centre in Mental Health Net (CIBERSAM), Santiago Apóstol Hospital, University of the Basque Country, 01004, Vitoria, Spain. 8. Department of Psychiatry, Puerta de Hierro University Hospital-Segovia de Arana Health Research Institute (IDIPHISA), Madrid, Spain. hmblasco@yahoo.es. 9. CIBERSAM, Madrid, Spain. hmblasco@yahoo.es. 10. Madrid Autonoma University, Madrid, Spain. hmblasco@yahoo.es.
Abstract
PURPOSE OF REVIEW: The current serotonin-based biological model of suicidal behavior (SB) may be too simplistic. There is emerging evidence that other biomarkers and biological systems may be involved in SB pathophysiology. The literature on the endocannabinoid (EC) systems and SB is limited. The objective of the present article is to review all available information on the relationship between cannabinoid receptors (CB1 and CB2 receptors), and SB and/or psychological pain. RECENT FINDINGS: Our review is limited by the small number and heterogeneity of studies identified: (1) an autopsy study describing elevated levels of CB1 receptor activity in the prefrontal cortex and suicide in both depression and alcoholism and (2) studies supporting the involvement of both CB1 and CB2 receptors in the regulation of neuropathic pain and stress-induced analgesia. We conclude that cannabinoid receptors, particularly CB1 receptors, may become promising targets for the development of novel therapeutic tools for the treatment of SB.
PURPOSE OF REVIEW: The current serotonin-based biological model of suicidal behavior (SB) may be too simplistic. There is emerging evidence that other biomarkers and biological systems may be involved in SB pathophysiology. The literature on the endocannabinoid (EC) systems and SB is limited. The objective of the present article is to review all available information on the relationship between cannabinoid receptors (CB1 and CB2 receptors), and SB and/or psychological pain. RECENT FINDINGS: Our review is limited by the small number and heterogeneity of studies identified: (1) an autopsy study describing elevated levels of CB1 receptor activity in the prefrontal cortex and suicide in both depression and alcoholism and (2) studies supporting the involvement of both CB1 and CB2 receptors in the regulation of neuropathic pain and stress-induced analgesia. We conclude that cannabinoid receptors, particularly CB1 receptors, may become promising targets for the development of novel therapeutic tools for the treatment of SB.
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