The endogenous cannabinoid system controls extinction of aversive memories

By G. Marsicano, Carsten T. Wotjak, S. Azad, T. Bisogno, G. Rammes, M. Cascio, Heike Hermann, Jianrong Tang, Clementine Hofmann, W. Zieglgänsberger and 2 more. Nature, 2002

1,735 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Cognitive Neuroscience, Pharmacology

View Paper: https://www.semanticscholar.org/paper/c1ec79606d812bfdce92ecf826d1e0ffb6c93b6b

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In Cellular and Molecular Neuroscience

In Cognitive Neuroscience

In Pharmacology

Citations in the corpus

Neurobiological Interactions Between Stress and the Endocannabinoid System (2016, background): “Over a decade ago, Marsicano et al (2002) and subsequent investigators demonstrated that genetic deletion of CB1 receptors, as well as systemic or intra-BLA inhibition of eCB transmission, robustly inhibits fear extinction (Chhatwal et al, 2005; Ganon-Elazar and Akirav, 2009; Marsicano et al, 2002;…”
Cannabinoid physiology and pharmacology: 30 years of progress. (2004, background): “These changes would be consistent with the role of endogenous cannabinoids in memory processes (Marsicano et al., 2002).”
Metaplasticity: tuning synapses and networks for plasticity (2008, background): “These receptors are activated by endogenous endocannabinoids that serve as retrograde signals following postsynaptic group-1 mGluR activation and membrane depolarizatio”
The endocannabinoid system drives neural progenitor proliferation (2005, positive): “Embryonic NPs from wild-type and CB1 knockout mice (19) was cultured (10,000 cells/ml) in the continuous presence of cannabinoids for the indicated number of passages (1 passage every 4 days).”
Cannabidiol as a Potential Treatment for Anxiety Disorders (2015, background): “Regarding conditioned fear, the effect of CB1R activation is complex: CB1R activation may enhance or reduce fear expression, depending on brain locus and the eCB ligand [34]; however, CB1R activation potently enhances fear extinction [35], and can prevent fear reconsolidation.”
Model organisms: The ascent of mouse: advances in modelling human depression and anxiety (2005, positive): “Failure to extinguish learned fear responses is another key feature of post-traumatic stress disorder, phobias and other anxiety disorders that is readily studied, but as yet underused, in genetically modified mic”
Extinction circuits for fear and addiction overlap in prefrontal cortex. (2009, background): “These effects parallel those of systemic administration of CB1 agents on fear extinction (Marsicano et al. 2002; Chhatwal et al. 2005; Pamplona et al. 2006).”
Selective blockade of 2-arachidonoylglycerol hydrolysis produces cannabinoid behavioral effects (2008, background): “The incorporation of a piperazine spacer and a distal bisaryl motif, as represented in WWL152 (8) and WWL162 (9) (Fig.”
Neural Mechanisms of Extinction Learning and Retrieval (2008, background): “Acquisition of extinction was also slowed by blockade of the cannabinoid CB1 receptor (Marsicano et al, 2002; Varvel et al, 2005) and accelerated by CB1 agonists or cannabinoid reuptake inhibitors (Chhatwal et al, 2005a; Pamplona et al, 2006).”
A Comprehensive Profile of Brain Enzymes that Hydrolyze the Endocannabinoid 2‐Arachidonoylglycerol (2007, background): “Endocannabinoid signaling has been found to modulate a number of physiological processes, including pain sensation [3], appetite [4], and cognitive and emotional state [5, 6].”
Neurons in medial prefrontal cortex signal memory for fear extinction (2002, background): “Separate extinction mechanisms are also indicated by pharmacological evidence: short-term memory for fear extinction seems to be independent of N -methyl- d -aspartate (NMDA) receptor”
The molecular logic of endocannabinoid signalling (2003, result): “This idea is further supported by two findings: first, presentation of anxiogenic stimuli increases anandamide and 2-AG concentrations in the mouse amygdal”