Source
http://www.ncbi.nlm.nih.gov/pubmed/21309120
Department of Pharmacology, Federal University of Minas Gerais, Av. António Carlos 6627, Belo Horizonte, MG 31270-901, Brazil.Abstract
The
term cannabinoids encompasses compounds produced by the plant Cannabis
sativa, such as delta9-tetrahydrocannabinol, and synthetic counterparts.
Their actions occur mainly through activation of cannabinoid type 1
(CB1) receptors. Arachidonoyl ethanolamide (anandamide) and
2-arachidonoyl glycerol (2-AG) serve as major endogenous ligands
(endocannabinoids) of CB1 receptors. Hence, the cannabinoid receptors,
the endocannabinoids, and their metabolizing enzymes comprise the
endocannabinoid system. Cannabinoids induce diverse responses on
anxiety- and fear-related behaviors. Generally, low doses tend to induce
anxiolytic-like effects, whereas high doses often cause the opposite.
Inhibition of endocannabinoid degradation seems to circumvent these
biphasic effects by enhancing CB1 receptor signaling in a temporarily
and spatially restricted manner, thus reducing anxiety-like behaviors.
Pharmacological blockade or genetic deletion of CB1 receptors, in turn,
primarily exerts anxiogenic-like effects and impairments in extinction
of aversive memories. Interestingly, pharmacological blockade of
Transient Receptor Potential Vanilloid Type-1 (TRPV1) channel, which can
be activated by anandamide as well, has diametrically opposite
consequences. This book chapter summarizes and conceptualizes our
current knowledge about the role of (endo)cannabinoids in fear and
anxiety and outlines implications for an exploitation of the
endocannabinoid system as a target for new anxiolytic drugs.
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