Skip to content

Role of cyclic AMP in the actions of cannabinoid receptors.

S R Childers, S A Deadwyler

Biochemical Pharmacology September 27, 1996 DOI: 10.1016/0006-2952(96)00419-4 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Review Peer reviewed
Key findings Argues that cannabinoids act principally through G-protein-coupled receptors, with G-protein activation as the initiating signaling step, and that inhibition of adenylyl cyclase is only one of several coupled effectors. Proposes that this inhibition contributes to cannabinoid functions including modulation of a voltage-dependent K+ channel ("A" current) in the hippocampus, and may also produce long-term gene-expression changes and inhibit anandamide synthesis.

Abstract

Cannabinoids, including delta 9-tetrahydrocannabinol (THC), bind to receptors that couple to Gi/o-proteins and inhibit adenylyl cyclase. However, like other G-protein-coupled receptors, cannabinoid receptors are also coupled to other effector systems. This review examines the characteristics of the cannabinoid-G-protein-adenylyl cyclase system, and explores the role of cyclic AMP in mediating effects of these drugs. Several conclusions emerge from this research. First, the principal actions of cannabinoids are mediated through G-protein-coupled receptors, and the intracellular signaling mechanism that initiates cellular response of cannabinoids is activation of G-proteins. Second, cannabinoid-inhibited adenylyl cyclase is only one of several different effectors coupled to these receptors, and different effectors may be used for different types of responses. Third, cannabinoid inhibition of adenylyl cyclase plays an important role in several aspects of cannabinoid function, including modulating conductance at a voltage-dependent K+ channel ("A" current) in the hippocampus, thus providing an effective rationale for behavioral effects of cannabinoids mediated in this region. Other functions of this system may include production of long-term changes in gene expression by inhibition of cyclic AMP response elements on strategic genes, and inhibition of anandamide synthesis, thus mediating some of the long-term effects of cannabinoids on neuronal function.

Citations in the library

Explore topics