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PubMed · 172034

Adenyl cyclase.

Abstract

Many hormones interact with their target cells by binding to receptors located on the external surface of the target cells' plasma membrane and subsequently stimulating the enzyme, adenyl cyclase, which is located within the plasma membrane. Stimulation of adenyl cyclase results in formation of cyclic AMP which is released from the membrane into the cell and acts within the cell to regulate a wide variety of cellular processes. In this review, the characteristics of hormone receptors and the relationship between receptor occupancy and adenyl cyclase stimulation are discussed. Our current understanding of the roles of hormones, substrate, magnesium, calcium, and guanine nucleotides as regulators of adenyl cyclase activity is summarized. Because of the central importance of adenyl cyclase and cyclic AMP as mediators of the cellular response to hormones, it is to be expected that many diseases may result from defects in this enzyme system. Indeed, several adenyl cyclase related diseases have been identified and the molecular bases for these diseases are discussed in this review.

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BibTeXRIS

M L Steer. 1975. Adenyl cyclase.. https://doi.org/10.1097/00000658-197511000-00012

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Adenylyl Cyclases↗

Chronic but not acute intracerebroventricular administration of amyloid beta-peptide(25-35) decreases somatostatin content, adenylate cyclase activity, somatostatin-induced inhibition of adenylate cyclase activity, and adenylate cyclase I levels in the rat hippocampus.

Although alterations in adenylate cyclase (AC) activity and somatostatin (SRIF) receptor density have been reported in Alzheimer's disease, the effects of amyloid beta-peptide (Abeta) on these parameters in the hippocampus are unknown. Our aim was to investigate whether the peptide fragment Abeta(25-35) can affect the somatostatinergic system in the rat hippocampus. Hence, Abeta(25-35) was injected intracerebroventricularly (i.c.v.) to Wistar rats in a single dose or infused via an osmotic minipump connected to a cannula implanted in the right lateral ventricle during 14 days. The animals were decapitated 7 or 14 days after the single injection and 14 days after chronic infusion of the peptide. Chronic i.c.v. infusion of Abeta(25-35) decreased SRIF-like immunoreactive content without modifying the SRIF receptor density, SRIF receptor expression, or the Gialpha(1), Gialpha(2), and Gialpha(3) protein levels in the hippocampus. This treatment, however, caused a decrease in basal and forskolin-stimulated AC activity as well as in the capacity of SRIF to inhibit AC activity. Furthermore, the protein levels of the neural-specific AC type I were significantly decreased in the hippocampus of the treated rats, whereas an increase in the levels of AC V/VI was found, with no alterations in type VIII AC. A single i.c.v. dose of Abeta(25-35) exerted no effect on SRIF content or SRIF receptors but induced a slight decrease in forskolin-stimulated AC activity and its inhibition by SRIF. Because chronic Abeta(25-35) infusion impairs learning and memory whereas SRIF facilitates these functions, the alterations described here might be physiologically important given the decreased cognitive behavior previously reported in Abeta-treated rats.

Adenylyl Cyclases↗

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Adenylyl Cyclases↗