Prostaglandins and the synergism between VIP and noradrenaline in the cerebral cortex

We have previously shown that vasoactive intestinal peptide (VIP) and noradrenaline (NA) interact synergistically to increase cyclic AMP levels in mouse cerebral cortical slices. The pharmacological mechanism of this synergism is the potentiation by NA, through alpha 1 adrenergic receptors, of the s...

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Bibliographic Details
Published in:Nature (London) 1987-08, Vol.328 (6131), p.637-640
Main Authors: Schaad, Nicolas C, Schorderet, Michel, Magistretti, Pierre J
Format: Article
Language:English
Subjects:
Animals
Arachidonic Acid
Arachidonic Acids - metabolism
Biochemistry and metabolism
Biological and medical sciences
Calcium - physiology
Central nervous system
Cerebral Cortex - drug effects
Cerebral Cortex - metabolism
Cyclic AMP - biosynthesis
Dinoprost
Dinoprostone
Drug Synergism
Fundamental and applied biological sciences. Psychology
Male
Mice
Mice, Inbred ICR
Norepinephrine - pharmacology
Phospholipases A - metabolism
Prostaglandins - pharmacology
Prostaglandins E - pharmacology
Prostaglandins F - pharmacology
Receptors, Adrenergic, alpha - physiology
Vasoactive Intestinal Peptide - pharmacology
Vertebrates: nervous system and sense organs
Citations: Items that cite this one
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Summary:We have previously shown that vasoactive intestinal peptide (VIP) and noradrenaline (NA) interact synergistically to increase cyclic AMP levels in mouse cerebral cortical slices. The pharmacological mechanism of this synergism is the potentiation by NA, through alpha 1 adrenergic receptors, of the stimulatory effect of VIP on cAMP formation. A similar interaction has been confirmed in guinea pig cerebral cortex and in discrete nuclei of the rat hypothalamus. Furthermore VIP and NA interact synergistically to depress the spontaneous activity of identified neurons in rat neocortex. At the cellular level, this synergistic interaction suggests that VIP- and NA-containing neuronal systems may converge, at least in part, on the same target cells to increase cAMP levels in the cerebral cortex. At the molecular level, the interaction may occur at various steps in signal transduction, between receptors, intramembrane transduction processes or intracellular effector mechanisms. Here we report that the alpha 1-adrenergic potentiation of the increases in cAMP elicited by VIP involves the formation of arachidonic acid metabolites and is mimicked by prostglandins F2 alpha and E2.
ISSN:0028-0836
1476-4687
DOI:10.1038/328637a0