Neuroregulatory and Neuropathological Actions of the Ether-Phospholipid Platelet-Activating Factor

Platelet-activating factor (PAF) is a naturally occurring phospholipid that serves as a critical mediator in diverse biological and pathophysiological processes. In this study of the interactions of PAF with neuronal cells, it was found that PAF increased the intracellular levels of free calcium ion...

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Bibliographic Details
Published in:Science (American Association for the Advancement of Science) 1988-06, Vol.240 (4860), p.1792-1794
Main Authors: Kornecki, Elizabeth, Ehrlich, Yigal H.
Format: Article
Language:English
Subjects:
Adrenergic Fibers - cytology
Animals
Atrial fibrillation
Benzodiazepines - pharmacology
Biochemistry
Biological and medical sciences
Calcium
Calcium (Chemical element)
Calcium - physiology
Calcium Channel Blockers - pharmacology
Cell Line
Cell lines
Cell physiology
Cell regulation
Cell Survival - drug effects
Cells
Cellular control mechanisms
Central nervous system
Cholinergic Fibers - cytology
Cultured cells
Feathers
Fundamental and applied biological sciences. Psychology
Growth factors
Molecular and cellular biology
neuroblastoma cells
Neurological disorders
Neurons
Neurons - cytology
Neurons - physiology
Neurotoxins
PC12 cells
pheochromocytoma cells
Phospholipid Ethers - pharmacology
Physiological aspects
Platelet activating factor
Platelet Activating Factor - pharmacology
Responses to growth factors, tumor promotors, other factors
Viability
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Summary:Platelet-activating factor (PAF) is a naturally occurring phospholipid that serves as a critical mediator in diverse biological and pathophysiological processes. In this study of the interactions of PAF with neuronal cells, it was found that PAF increased the intracellular levels of free calcium ions in cells of the clones NG108-15 and PC12. The increase was dependent on extracellular calcium and was inhibited by the antagonistic PAF analog CV-3988 and by the calcium-influx blockers prenylamine and diltiazem. A functional consequence of this interaction was revealed by measuring a PAF-elicited, Ca$^{2+}$-dependent secretion of adenosine triphosphate from PC12 cells. Exposure of NG108-15 cells for 3 to 4 days to low concentrations of PAF induced neuronal differentiation; higher concentrations were neurotoxic. Thus, by influencing Ca$^{2+}$ fluxes, PAF may play a physiological role in neuronal development and a pathophysiological role in the degeneration that occurs when neurons are exposed to circulatory factors as a result of trauma, stroke, or spinal cord injury.
ISSN:0036-8075
1095-9203
DOI:10.1126/science.3381103