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

Nicolas C. Schaad; Michel Schorderet; Pierre J. Magistretti

doi:10.1038/328637a0

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

Nicolas C. Schaad, Michel Schorderet, Pierre J. Magistretti^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

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Abstract

We have previously shown that vasoactive intestinal peptide (VIP) and noradrenaline (NA) interact synergistically to increase cyclic AMP levels in mouse cerebral cortical slices¹. The pharmacological mechanism of this synergism is the potentiatioh by NA, through α₁ adrenergic receptors, of the stimulatory effect of VIP on cAMP formation². A similar interaction has been confirmed in guinea pig cerebral cortex³ and in discrete nuclei of the rat hypothalamus⁴. Furthermore VIP and NA interact synergistically to depress the spontaneous activity of identified neurons in rat neocortex⁵. 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 α₁-adrenergic potentiation of the increases in cAMP elicited by VIP involves the formation of arachidonic acid metabolites and is mimicked by prostglandins F₂α and E₂.

Original language	English (US)
Pages (from-to)	637-640
Number of pages	4
Journal	NATURE
Volume	328
Issue number	6131
DOIs	https://doi.org/10.1038/328637a0
State	Published - 1988
Externally published	Yes

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title = "Prostaglandins and the synergism between VIP and noradrenaline in the cerebral cortex",

abstract = "We have previously shown that vasoactive intestinal peptide (VIP) and noradrenaline (NA) interact synergistically to increase cyclic AMP levels in mouse cerebral cortical slices1. The pharmacological mechanism of this synergism is the potentiatioh by NA, through α1 adrenergic receptors, of the stimulatory effect of VIP on cAMP formation2. A similar interaction has been confirmed in guinea pig cerebral cortex3 and in discrete nuclei of the rat hypothalamus4. Furthermore VIP and NA interact synergistically to depress the spontaneous activity of identified neurons in rat neocortex5. 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 α1-adrenergic potentiation of the increases in cAMP elicited by VIP involves the formation of arachidonic acid metabolites and is mimicked by prostglandins F2α and E2.",

author = "Schaad, {Nicolas C.} and Michel Schorderet and Magistretti, {Pierre J.}",

year = "1988",

doi = "10.1038/328637a0",

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AU - Schaad, Nicolas C.

AU - Schorderet, Michel

AU - Magistretti, Pierre J.

PY - 1988

Y1 - 1988

N2 - We have previously shown that vasoactive intestinal peptide (VIP) and noradrenaline (NA) interact synergistically to increase cyclic AMP levels in mouse cerebral cortical slices1. The pharmacological mechanism of this synergism is the potentiatioh by NA, through α1 adrenergic receptors, of the stimulatory effect of VIP on cAMP formation2. A similar interaction has been confirmed in guinea pig cerebral cortex3 and in discrete nuclei of the rat hypothalamus4. Furthermore VIP and NA interact synergistically to depress the spontaneous activity of identified neurons in rat neocortex5. 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 α1-adrenergic potentiation of the increases in cAMP elicited by VIP involves the formation of arachidonic acid metabolites and is mimicked by prostglandins F2α and E2.

AB - We have previously shown that vasoactive intestinal peptide (VIP) and noradrenaline (NA) interact synergistically to increase cyclic AMP levels in mouse cerebral cortical slices1. The pharmacological mechanism of this synergism is the potentiatioh by NA, through α1 adrenergic receptors, of the stimulatory effect of VIP on cAMP formation2. A similar interaction has been confirmed in guinea pig cerebral cortex3 and in discrete nuclei of the rat hypothalamus4. Furthermore VIP and NA interact synergistically to depress the spontaneous activity of identified neurons in rat neocortex5. 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 α1-adrenergic potentiation of the increases in cAMP elicited by VIP involves the formation of arachidonic acid metabolites and is mimicked by prostglandins F2α and E2.

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ER -

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

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