Lee E. Limbird

TL;DR: The hypotensive response to α2AR agonists was lost in the mutant mice, demonstrating that the α2aAR subtype plays a principal role in this response.

TL;DR: It is demonstrated that alpha2AR agonist-elicited sedative, anesthetic-sparing, and analgesic responses are lost in a mouse line expressing a subtly mutated alpha2AAR, D79N alpha2 aAR, created by two-step homologous recombination, providing definitive evidence that the alpha1AAR subtype is the primary mediator of clinically important central actions of alpha2 AR agonists.

TL;DR: The results indicate that the alpha2A-AR is a major presynaptic receptor subtype regulating norepinephrine release from sympathetic nerves; however, the residual alpha2-mediated effect in the alpha1-AR knockout mice suggests that a second alpha2 subtype (alpha2B or alpha2C) also functions as a presynptic autoreceptor to inhibit transmitter release.

TL;DR: Introduction to Receptor Theory - Origin of the Receptor Concept - Occupancy Theory -Relationship Between Occupancy and Response - Concept of Spare Receptors - Operational Models of Pharmacological Agonism - Rate Theory - Allosteric Theory - Beyond Two-State Receptor theory.

TL;DR: This review summarizes the current understanding of how these receptors are coupled to their multiple potential effector mechanisms and offers some speculation about the possible interplay between the biochemical and electrophysiological sequels of receptor occupancy.