Abstract
Following the discovery of the endocannabinoid system and its potential as a therapeutic target for various pathological conditions, growing interest led researchers to investigate the role of cannabis and its derivatives for medical purposes. The compounds Δ9-tetrahydrocannabinol and cannabidiol are the most abundant phytocannabinoids found in cannabis extracts, as well as the most studied. The present review aims to provide an overview of the current evidence for their beneficial effects in treating psychiatric disorders, including schizophrenia, anxiety, and depression. Nevertheless, further investigations are required to clarify many pending issues, especially those relative to the assessment of benefits and risks when using cannabis for therapeutic purposes, thereby also helping national and federal jurisdictions to remain updated.
Highlights
Evidence of the consumption of cannabis for therapeutic uses is prevalent throughout history
The present review addresses the current literature on the endocannabinoid system in the neurobiology of psychiatric disorders
Despite the growing knowledge base of neuropsychiatric disorder neurobiology, a high percentage of patients do not respond to first-line therapeutic interventions
Summary
Evidence of the consumption of cannabis for therapeutic uses is prevalent throughout history. AEA and 2-AG are immediately released by the postsynaptic terminal and activate cannabinoid receptors (CBRs) in the presynaptic membrane, inhibiting neurotransmission release by activating presynaptic K+ channels and inhibiting N- and P/Q-type Ca2+ channels [23]. The compound 2-AG is metabolized into arachidonic acid and glycerol mainly by the enzyme monoacylglycerol lipase (MAGL) [23] These metabolic pathways represent the key points in the regulation of endocannabinoid tissue levels. Synaptic AEA level:isendocannabinoids are produced upon demand after cellular depolarization from lipid derived mainly from NAPE by a specific phospholipase D; 2-AG is primarily formed from precursors. EndocannabinoidFAAH: signaling terminated by monoacylglycerol lipase; DAG: diacylglycerol; NAPE:2-AG: N-acyl-phosphatidylethanolamine; metabolicMGL: degradation by specific enzymes. NAPE-PLD: N-acyl-phosphatidylethanolamine phospholipase D; CBR: receptor; Gi/o: G protein; Ca2+: calcium; K+: potassium
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