Endocannabinoid lipids and mediated system: implications for alcoholism and neuropsychiatric disorders.
K Yaragudri Vinod, Basalingappa L Hungund
Life Sciences August 19, 2005 DOI: 10.1016/j.lfs.2005.05.041 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Review Peer reviewed |
|---|---|
| Key findings | The authors argue that the endocannabinoid system participates in the pathophysiology of alcoholism, schizophrenia, depression, and suicide. They report that chronic ethanol exposure alters endocannabinoid synthesis, precursor levels, and CB1 receptor density and coupling efficacy, while noting that evidence for the EC system's role in neuropsychiatric disorders is still emerging. |
Abstract
Several natural lipids have emerged as candidate modulators of central nervous system (CNS) functions. Fatty acid amides and their coupled signaling pathways are known to regulate several physiological and behavioral processes. Recent studies from our laboratory and others also have implicated endogenous marijuana-like brain constituents, endocannabinoids (ECs), and cannabinoid-1 (CB1) receptors in the neural circuitry that mediate drug addiction and neuropsychiatric disorders. Neuroadaptation to chronic ethanol (EtOH) has been shown to involve changes in the EC system. These changes include alterations in the synthesis of EC, their precursors, as well as density and coupling efficacy of CB1 receptors. The evidence for the participation of the EC system in the pathophysiology of various neuropsychiatric disorders is just beginning to evolve. It is of great interest to explore the components of EC system in different areas of the CNS for further understanding of its role in health and disease. This article presents a comprehensive overview of the currently available literature pertaining to the role of the EC system in alcoholism, schizophrenia, depression and/or suicide.
Citations in the library
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