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      Cannabidiol as a Potential Treatment for Anxiety Disorders

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          Abstract

          Cannabidiol (CBD), a Cannabis sativa constituent, is a pharmacologically broad-spectrum drug that in recent years has drawn increasing interest as a treatment for a range of neuropsychiatric disorders. The purpose of the current review is to determine CBD’s potential as a treatment for anxiety-related disorders, by assessing evidence from preclinical, human experimental, clinical, and epidemiological studies. We found that existing preclinical evidence strongly supports CBD as a treatment for generalized anxiety disorder, panic disorder, social anxiety disorder, obsessive–compulsive disorder, and post-traumatic stress disorder when administered acutely; however, few studies have investigated chronic CBD dosing. Likewise, evidence from human studies supports an anxiolytic role of CBD, but is currently limited to acute dosing, also with few studies in clinical populations. Overall, current evidence indicates CBD has considerable potential as a treatment for multiple anxiety disorders, with need for further study of chronic and therapeutic effects in relevant clinical populations.

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          The online version of this article (doi:10.1007/s13311-015-0387-1) contains supplementary material, which is available to authorized users.

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          Dissociable roles of prelimbic and infralimbic cortices, ventral hippocampus, and basolateral amygdala in the expression and extinction of conditioned fear.

          Demetrio Sierra-Mercado, Gregory J. Quirk, Nancy Padilla-Coreano (2011)
          Current models of conditioned fear expression and extinction involve the basolateral amygdala (BLA), ventral medial prefrontal cortex (vmPFC), and the hippocampus (HPC). There is some disagreement with respect to the specific roles of these structures, perhaps due to subregional differences within each area. For example, growing evidence suggests that infralimbic (IL) and prelimbic (PL) subregions of vmPFC have opposite influences on fear expression. Moreover, it is the ventral HPC (vHPC), rather than the dorsal HPC, that projects to vmPFC and BLA. To help determine regional specificity, we used small doses of the GABA(A) agonist muscimol to selectively inactivate IL, PL, BLA, or vHPC in an auditory fear conditioning and extinction paradigm. Infusions were performed prior to extinction training, allowing us to assess the effects on both fear expression and subsequent extinction memory. Inactivation of IL had no effect on fear expression, but impaired the within-session acquisition of extinction as well as extinction memory. In contrast, inactivation of PL impaired fear expression, but had no effect on extinction memory. Inactivation of the BLA or vHPC impaired both fear expression and extinction memory. Post-extinction inactivations had no effect in any structure. We suggest a model in which amygdala-dependent fear expression is modulated by inputs from PL and vHPC, whereas extinction memory requires extinction-induced plasticity in IL, BLA, and/or vHPC.
          Article 0 comments Cited 370 times – based on 0 reviews     Review now
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            The endogenous cannabinoid system controls extinction of aversive memories.

            Giovanni Marsicano, Carsten Wotjak, Shahnaz Azad … (2002)
            Acquisition and storage of aversive memories is one of the basic principles of central nervous systems throughout the animal kingdom. In the absence of reinforcement, the resulting behavioural response will gradually diminish to be finally extinct. Despite the importance of extinction, its cellular mechanisms are largely unknown. The cannabinoid receptor 1 (CB1) and endocannabinoids are present in memory-related brain areas and modulate memory. Here we show that the endogenous cannabinoid system has a central function in extinction of aversive memories. CB1-deficient mice showed strongly impaired short-term and long-term extinction in auditory fear-conditioning tests, with unaffected memory acquisition and consolidation. Treatment of wild-type mice with the CB1 antagonist SR141716A mimicked the phenotype of CB1-deficient mice, revealing that CB1 is required at the moment of memory extinction. Consistently, tone presentation during extinction trials resulted in elevated levels of endocannabinoids in the basolateral amygdala complex, a region known to control extinction of aversive memories. In the basolateral amygdala, endocannabinoids and CB1 were crucially involved in long-term depression of GABA (gamma-aminobutyric acid)-mediated inhibitory currents. We propose that endocannabinoids facilitate extinction of aversive memories through their selective inhibitory effects on local inhibitory networks in the amygdala.
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              Endocannabinoid signaling and synaptic function.

              Pablo E. Castillo, Thomas Younts, Andrés Chávez … (2012)
              Endocannabinoids are key modulators of synaptic function. By activating cannabinoid receptors expressed in the central nervous system, these lipid messengers can regulate several neural functions and behaviors. As experimental tools advance, the repertoire of known endocannabinoid-mediated effects at the synapse, and their underlying mechanism, continues to expand. Retrograde signaling is the principal mode by which endocannabinoids mediate short- and long-term forms of plasticity at both excitatory and inhibitory synapses. However, growing evidence suggests that endocannabinoids can also signal in a nonretrograde manner. In addition to mediating synaptic plasticity, the endocannabinoid system is itself subject to plastic changes. Multiple points of interaction with other neuromodulatory and signaling systems have now been identified. In this Review, we focus on new advances in synaptic endocannabinoid signaling in the mammalian brain. The emerging picture not only reinforces endocannabinoids as potent regulators of synaptic function but also reveals that endocannabinoid signaling is mechanistically more complex and diverse than originally thought. Copyright © 2012 Elsevier Inc. All rights reserved.
              Article 0 comments Cited 337 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Esther M. Blessing: esther.blessing@nyumc.org
                Journal
                Journal ID (nlm-ta): Neurotherapeutics
                Journal ID (iso-abbrev): Neurotherapeutics
                Title: Neurotherapeutics
                Publisher: Springer US (New York )
                ISSN (Print): 1933-7213
                ISSN (Electronic): 1878-7479
                Publication date (Electronic): 4 September 2015
                Publication date (Print): October 2015
                Volume: 12
                Issue: 4
                Pages: 825-836
                Affiliations
                [1 ]New York University School of Medicine, New York, NY USA
                [2 ]Instituto de Neurociencias de Alicante, Universidad Miguel Hernández and Consejo Superior de Investigaciones Científicas, Alicante, Spain
                Article
                Accession ID: PMC4604171 Pmcid ID: PMC4604171 Pmc-uid ID: 4604171 Publisher ID: 387
                DOI: 10.1007/s13311-015-0387-1
                PMC ID: 4604171
                PubMed ID: 26341731
                SO-VID: c9d9c38e-aa81-4d49-80e6-42d5d92b23c0
                Copyright © © The American Society for Experimental NeuroTherapeutics, Inc. 2015
                History
                Categories
                Subject: Review
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                issue-copyright-statement © The American Society for Experimental NeuroTherapeutics, Inc. 2015

                Keywords: Endocannabinoids,Generalized anxiety disorder,Post-traumatic stress disorder,Cannabidiol,Anxiety
                Data availability:
                Keywords: Endocannabinoids, Generalized anxiety disorder, Post-traumatic stress disorder, Cannabidiol, Anxiety

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