Abstract
Olfaction has a direct influence on behavior and cognitive processes. There are different neuromodulatory systems in olfactory circuits that control the sensory information flowing through the rest of the brain. The presence of the cannabinoid type-1 (CB1) receptor, (the main cannabinoid receptor in the brain), has been shown for more than 20 years in different brain olfactory areas. However, only over the last decade have we started to know the specific cellular mechanisms that link cannabinoid signaling to olfactory processing and the control of behavior. In this review, we aim to summarize and discuss our current knowledge about the presence of CB1 receptors, and the function of the endocannabinoid system in the regulation of different olfactory brain circuits and related behaviors.
Highlights
INSERM, U1215 NeuroCentre Magendie, 146 rue Léo Saignat, CEDEX, 33077 Bordeaux, France; University of Bordeaux, 146 rue Léo Saignat, 33000 Bordeaux, France
cannabinoid type-1 (CB1) and CB2 receptors belong to the superfamily of G-protein-coupled receptors (GPCRs) that consist of seven transmembrane domains with an extracellular N-terminal and an intracellular C-terminal tail [3]
The involvement of CB1 receptors in specific odor-related processes has been reported in specialized olfactory structures such as the olfactory epithelium (OE; [24,25,26,27]), the main olfactory bulb (MOB; [18,28,29,30,31,32,33,34]), and the piriform cortex (PC; [35,36,37,38,39,40]), and in other brain areas processing olfactory information [41,42,43,44]
Summary
Known as marijuana or cannabis, has been used for thousands of years for its therapeutic and recreational properties. CB1 and CB2 receptors belong to the superfamily of G-protein-coupled receptors (GPCRs) that consist of seven transmembrane domains with an extracellular N-terminal and an intracellular C-terminal tail [3]. Endocannabinoids can be synthesized, but not exclusively [4], by post-synaptic intracellular calcium elevations, which can be caused by various stimuli, including depolarization, the activation of metabotropic acetylcholine, and glutamate receptors, Gq-coupled receptors (i.e., M1/M3 and mGluR 1/5) [3]. The main effect of CB1 receptor activation is a decrease in neurotransmitter release, inducing different forms of endocannabinoid-mediated plasticity [3], such as the depolarization-. CB1 receptors are widely expressed in the central nervous system and likely represent the most abundant GPCR in the brain [15]. Given its ubiquitous expression in multiple brain areas, CB1 receptors modulate a variety of functions, from sensory perception to more complex cognitive processes such as learning and memory [16,17,18]
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