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The **cannabinoid signaling pathway** refers to the set of molecular mechanisms and signal transduction events regulated by activation of cannabinoid receptors, primarily CB1 and CB2, which are *G protein-coupled receptors*. CB1 is highly expressed in the central nervous system and mediates effects on mood, memory, pain, appetite, and various neuroendocrine functions. CB2 is mostly expressed on immune cells and mediates immunomodulation, inflammation, and pain relief. Both receptors are activated by endogenously produced cannabinoids (anandamide, 2-AG), phytocannabinoids (THC, CBD), and synthetic drugs. Their activation influences intracellular signaling pathways such as inhibition of adenylyl cyclase, modulation of MAP kinase pathways, and the regulation of neurotransmitter release, cell proliferation, and apoptosis. Dysregulation of this pathway is implicated in numerous diseases, and the receptors themselves are considered important therapeutic targets. However, "cannabinoid signaling pathway" is not itself a molecular entity but a collection of processes governed by defined receptor molecules[1][3][4][5].
Agonism of CB1/CB2 receptors (for THC, synthetic cannabinoids, endogenous ligands like anandamide and 2-AG) Antagonism/inverse agonism of CB1 receptor (for rimonabant) Modulation of adenylate cyclase inhibition Regulation of ion channel activity (CB1) MAPK pathway modulation Immune cell function modulation (CB2) Retrograde signaling modulation (CB1 in CNS)
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