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Cannabinoid receptor 1 (CB1), is a G protein-coupled cannabinoid receptor that in humans is encoded by the CNR1 gene. [5] And discovered, by determination and characterization in 1988, [6] and cloned in 1990 for the first time. [7] [8] [9] The human CB1 receptor is expressed in the peripheral nervous system and central nervous system. [5]
The existence of cannabinoid receptors in the brain was discovered from in vitro studies in the 1980s, with the receptor designated as the cannabinoid receptor type 1 or CB1. [14] [15] The DNA sequence that encodes a G-protein-coupled cannabinoid receptor in the human brain was identified and cloned in 1990.
The cannabinoid receptors CB 1 and CB 2, two G protein-coupled receptors that are located in the central and peripheral nervous systems. The neurons, neural pathways, and other cells where these molecules, enzymes, and one or both cannabinoid receptor types are all localized together collectively comprise the endocannabinoid system.
The discovery of the first cannabinoid receptors in the 1980s helped to resolve this debate. [10] These receptors are common in animals. Two known cannabinoid receptors are termed CB 1 and CB 2, [11] with mounting evidence of more. [12] The human brain has more cannabinoid receptors than any other G protein-coupled receptor (GPCR) type. [13]
The cannabinoid receptor 2 (CB2), is a G protein-coupled receptor from the cannabinoid receptor family that in humans is encoded by the CNR2 gene. [5] [6] It is closely related to the cannabinoid receptor 1 (CB1), which is largely responsible for the efficacy of endocannabinoid-mediated presynaptic-inhibition, the psychoactive properties of tetrahydrocannabinol (THC), the active agent in ...
Depolarization-induced suppression of inhibition is the classical and original electrophysiological example of endocannabinoid function in the central nervous system.Prior to the demonstration that depolarization-induced suppression of inhibition was dependent on the cannabinoid CB1 receptor function, there was no way of producing an in vitro endocannabinoid mediated effect.
GPR55 is activated by the plant cannabinoids Δ 9-THC [12] and the endocannabinoids anandamide, 2-AG and noladin ether in the low nanomolar range. Exocannabinoids such as the synthetic cannabinoid CP-55940 are also able to activate the receptor [12] while the structurally unrelated cannabinoid mimic WIN 55,212-2 fails to activate the receptor. [10]
Activation of CB1 enhances AMT activity through increased nitric oxide synthase (NOS) activity and subsequent increase of NO production, whereas AMT activity instead is reduced by activation of the CB2 cannabinoid receptor, which inhibits NOS and NO release, also suggesting the distribution of these receptors may drive AEA directional transport ...