The molecular logic of endocannabinoid signalling

By Daniele Piomelli. Nature Reviews Neuroscience, 2003

1,981 citations recorded by the source corpus.

The endocannabinoids are a family of lipid messengers that engage the cell surface receptors that are targeted by Δ9-tetrahydrocannabinol, the active principle in marijuana (Cannabis). They are made on demand through cleavage of membrane precursors and are involved in various short-range signalling processes. In the brain, they combine with CB1 cannabinoid receptors on axon terminals to regulate ion channel activity and neurotransmitter release. Their ability to modulate synaptic efficacy has a wide range of functional consequences and provides unique therapeutic possibilities.

Subfields: Cellular and Molecular Neuroscience, Pharmacology, Surgery

View Paper: https://www.semanticscholar.org/paper/1395aed014a2918967751d30000bb3f22a17e01d

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Citations in the corpus

The endocannabinoid system controls key epileptogenic circuits in the hippocampus. (2006, neutral): “The endocannabinoid system is an important neuromodulatory system involved in a plethora of physiological functions (De Petrocellis et al., 2004; Freund et al., 2003; Piomelli, 2003).”
Psychobiotics: a novel class of psychotropic. (2013, background): “Endocannabinoids are lipid molecules that act as neurotransmitters/neuromodulators in the brain, which contains specific receptors (15).”
Dendritic excitability and synaptic plasticity. (2008, positive): “Dendritic spikes have also been implicated in a relatively short-lasting form of synaptic plasticity, such as DSE, which is mediated by retrograde endocannabinoid signaling from the postsynaptic cell (128, 225, 394, 601, 842) (sect.”
Synaptic Plasticity: Multiple Forms, Functions, and Mechanisms (2008, background): “A major advance over the last decade has been the demonstration of the existence of endogenous cannabinoids (termed endocannabinoids) and their roles in modulating synaptic function (Chevaleyre et al, 2006; Freund et al, 2003; Kreitzer and Regehr, 2002; Piomelli, 2003; Wilson and Nicoll, 2002).”
The Endocannabinoid System as an Emerging Target of Pharmacotherapy (2006, background): “Stimulation of postsynaptic neurons is known to trigger the ondemand synthesis of endocannabinoids via an increase in intracellular calcium and/or stimulation of metabotropic receptors (reviewed in Piomelli, 2003; Lutz, 2004).”
Activation of the peripheral endocannabinoid system in human obesity. (2005, background): “Intracellular degradation by the enzyme fatty acid amide hydrolase (FAAH) limits endocannabinoid action (10).”
The tempted brain eats: pleasure and desire circuits in obesity and eating disorders. (2010, positive): “…to act in part as a reverse neurotransmitter, which could be released by an intrinsic spiny neuron in the shell to float back to nearby presynaptic axon terminals and stimulate CB1 receptors, and possibly modulate pre-synaptic opioid release (Cota et al., 2006; Kirkham, 2008; Piomelli, 2003).”
The endocannabinoid system and its therapeutic exploitation (2004, neutral): “Functions of the endocannabinoid system The components ( Figs 3 , 4 ) and possible physiological functions of the endocannabinoid system have been extensively reviewed in recent article”
Cannabinoid-based drugs as anti-inflammatory therapeutics (2005, background): “The naturally occurring endocannabinoids are produced by the cleavage of membrane fatty acid”
Endocannabinoid signaling and synaptic function (2012, background): “An enormous amount of information on the general properties of the eCB system has accumulated over the last two decades (for general reviews on the eCB system, see Ahn et al., 2008; Di Marzo, 2009; Howlett et al., 2002; Pertwee et al., 2010; Piomelli, 2003).”
Cannabinoid physiology and pharmacology: 30 years of progress. (2004, background): “In the hippocampus, DSI is initiated by depolarization-induced opening of N-type voltage-controlled Ca channels (VCCs) (Wilson and Nicoll, 2002), which in turn effects release of endocannabinoids via a Ca dependent process (Piomelli, 2003).”
A Comprehensive Profile of Brain Enzymes that Hydrolyze the Endocannabinoid 2‐Arachidonoylglycerol (2007, background): “The lipid transmitters anandamide (AEA) and 2-arachidonoylglycerol (2-AG) are referred to as ‘‘endocannabinoids’’ because they serve as natural ligands for the cannabinoid (CB) receptors, which are also targets of the psychoactive component of marijuana, D(9)-tetrahydrocannibinol [1, 2].”
The endocannabinoid system drives neural progenitor proliferation (2005, positive): “Keywords: cannabinoid • CB1 receptor • NP annabinoids and their endogenous counterparts, the endocannabinoids (eCBs), exert their actions in the brain through activation of the seven-transmembrane receptor CB1 (1, 2).”
Endocannabinoid signaling as a synaptic circuit breaker in neurological disease (2008, background): “In fact, CB 1 , the first cannabinoid receptor, is the most abundant G protein–coupled receptor in the brai”
Distinct coincidence detectors govern the corticostriatal spike timing‐dependent plasticity (2010, background): “In the striatum, mGluR5, M1Rs, PLCβ1 and DGLα are widely distributed on the somatodendritic surface of MSNs and are physically apposed to presynaptic CB1Rs (Narushima et al. 2007; Uchigashima et al. 2007; Fukaya et al. 2008).”
Cannabidiol enhances anandamide signaling and alleviates psychotic symptoms of schizophrenia (2012, background): “messengers that target the same cell surface receptors engaged by D(9)-tetrahydrocannabinol in marijuana.(2) Because D(9)-tetrahydrocannabinol and other direct-acting cannabinoid agonists can induce psychotic symptoms both in healthy volunteers and schizophrenic patients,(6,7) it has been suggested ”