Cannabinoid Receptor (CB1) (H6) rabbit mAb

The CB1 cannabinoid receptor was discovered in 1988 (1) and subsequently cloned (2) on the basis of its responsiveness to (−)-Δ⁹-tetrahydrocannabinol (Δ⁹-THC). Δ⁹-THC is the primary psychoactive constituent in Cannabis (marijuana), hence the name “cannabinoid” receptor was coined. CB1 is a member of the G-protein coupled receptor (GPCR) family. An arachidonic acid metabolite, N-arachidonylethanolamide and 2-arachidonoylglycerol (2-AG) was found to activated CB1 receptor (3). The second cannabinoid receptor (CB2) was isolated from differentiated myeloid cells. The CB2 receptor shares 44% amino acid homology with CB1, and a distinct yet similar binding profile, thus representing a receptor subtype. 

The CB1 receptor is one of the most abundant GPCRs in the brain; it is highly expressed in the basal ganglia nuclei, hippocampus, cortex and cerebellum (5,6). The CB1 distribution within the central nervous system correlates with its role in the control of motor function, cognition and memory, and analgesia. CB1 receptors are primarily localized to the terminals of central and peripheral neurons, where they mediate inhibition of neurotransmitter release (7). CB1 receptors are found in higher levels on GABAergic than glutamatergic neurons in various brain regions. CB1 receptors are also present on astrocytes, where they are expressed at much lower levels than on neurons; but where they have been shown to modulate synaptic transmission and plasticity (8,9).  The CB2 receptor is expressed in peripheral organs with immune function, including macrophages, spleen, tonsils, thymus, and leukocytes, as well as the lung and testes (10). Initial studies suggested that CB2 receptors were absent from the healthy brain (11).