Related Experiment Video
Updated: Aug 8, 2026
06:32
Dynamic Multiparameter Platelet Function Assessment Using a Capacitive Biosensor
Published on: May 2, 2025
[Platelet adenylate cyclase activity in alcoholics]
T Saito1, M Watanabe, Y Katamura
1Department of Neuropsychiatry, Sapporo Medical College, Hokkaido, Japan.
Arukoru Kenkyu to Yakubutsu Izon = Japanese Journal of Alcohol Studies & Drug Dependence
|December 1, 1992
Summary
Long-term abstinent alcoholics show reduced platelet adenylate cyclase (AC) activity when stimulated by ethanol. This finding suggests platelet AC activity could serve as a biological marker for alcoholism.
Area of Science:
- Biochemistry
- Neuroscience
- Addiction Research
Context:
- Alcoholism is a chronic relapsing disease with complex biological underpinnings.
- Understanding the long-term physiological changes associated with alcohol abstinence is crucial.
- Platelets offer a readily accessible model for studying cellular responses relevant to alcoholism.
Purpose:
- To investigate platelet adenylate cyclase (AC) activity in individuals with long-term alcohol abstinence.
- To determine if ethanol-induced AC activity in vitro differs between abstinent alcoholics and controls.
- To explore the potential of platelet AC activity as a biomarker for alcoholism.
Summary:
- Platelet adenylate cyclase (AC) activity was assessed in individuals abstinent from alcohol for over one year.
- While guanine nucleotide-stimulated AC activity remained unchanged, ethanol-induced AC activity was significantly reduced in abstinent alcoholics.
- These alterations in platelet AC response to ethanol suggest a persistent physiological change related to prior alcohol dependence.
Impact:
- Platelet AC activity may represent a potential biological marker for identifying individuals with a history of alcoholism.
- This research could contribute to developing objective measures for assessing alcohol use disorders.
- Findings may inform future therapeutic strategies targeting cellular signaling pathways affected by chronic alcohol exposure.
Related Concept Videos
01:09GPCRs Regulate Adenylyl Cylase Activity
Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...
Two...
01:25cAMP-dependent Protein Kinase Pathways
Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
01:22Formation of the Platelet Plug
The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...