Aminergic G protein-coupled receptors (Aminergic GPCRs)

Aminergic G protein-coupled receptors (GPCRs) represent a major subfamily of the Class A (rhodopsin-like) GPCRs, characterized by their ability to bind biogenic amine neurotransmitters such as dopamine, serotonin, histamine, epinephrine, and norepinephrine [1]. These receptors are integral to the regulation of a vast array of physiological processes, including cardiovascular function, respiratory control, and complex behaviors such as mood, sleep, and cognition [2]. Structurally, they possess a conserved seven-transmembrane domain architecture with a specific orthosteric binding pocket that accommodates the protonated amine group of their endogenous ligands [3]. Due to their pervasive role in human physiology, aminergic GPCRs are among the most heavily exploited therapeutic targets, accounting for a significant percentage of all FDA-approved drugs [2]. Pharmacological intervention typically involves small molecules that act as agonists, antagonists, or inverse agonists to correct signaling imbalances associated with diseases like schizophrenia, depression, and hypertension [4]. However, the high degree of structural homology within this family often leads to polypharmacology, which can result in both therapeutic benefits and adverse side effects [3]. Sources: [1] Alexander SP, et al. (2023). "The Concise Guide to PHARMACOLOGY 2023/24: G protein-coupled receptors." British Journal of Pharmacology. [2] Hauser AS, et al. (2017). "Trends in GPCR drug discovery: new agents, targets and indications." Nature Reviews Drug Discovery. [3] Michino M, et al. (2015). "What can crystal structures of aminergic receptors tell us about polypharmacology?" Trends in Pharmacological Sciences. [4] Roth BL, et al. (2017). "Structure-guided discovery of genetic and chemical probes for GPCRs." Neuron.

Other names

Biogenic amine receptorsMonoamine receptorsClass Am GPCRsAmine GPCRs

Modulation of intracellular signaling through G protein coupling (Gs, Gi/o, Gq/11) or beta-arrestin recruitment via agonism, antagonism, or inverse agonism of biogenic amine binding sites.