Mechanisms of VIP-Induced Neuroprotection against Neonatal Excitotoxicity

:  Two VIP receptors, shared with a similar affinity by pituitary adenylate cyclase‐activating polypeptide (PACAP), have been cloned: VPAC1 and VPAC2. PHI binds to these receptors with a lower affinity. We previously showed that VIP protects against excitotoxic white matter damage in newborn mice. T...

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Bibliographic Details
Published in:Annals of the New York Academy of Sciences 2006-07, Vol.1070 (1), p.512-517
Main Authors: RANGON, CLAIRE-MARIE, DICOU, ELENI, GOURSAUD, STÉPHANIE, MOUNIEN, LOURDES, JÉGOU, SYLVIE, JANET, THIERRY, MULLER, JEAN-MARC, LELIÈVRE, VINCENT, GRESSENS, PIERRE
Format: Article
Language:English
Subjects:
Animals
Animals, Newborn
BDNF
Brain - drug effects
Brain-Derived Neurotrophic Factor - genetics
Data processing
Mice
Neurons - drug effects
Neurons - metabolism
Neuroprotective Agents - pharmacology
Neurotoxins - pharmacology
PACAP
PHI
Pituitary Adenylate Cyclase-Activating Polypeptide - pharmacology
PKC
Receptors, Vasoactive Intestinal Peptide, Type II - metabolism
Vasoactive Intestinal Peptide - pharmacology
VPAC2
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Summary::  Two VIP receptors, shared with a similar affinity by pituitary adenylate cyclase‐activating polypeptide (PACAP), have been cloned: VPAC1 and VPAC2. PHI binds to these receptors with a lower affinity. We previously showed that VIP protects against excitotoxic white matter damage in newborn mice. This article aimed to determine the receptor involved in VIP‐induced neuroprotection. VIP effects were mimicked with a similar potency by VPAC2 agonists and PHI but not by VPAC1 agonists, PACAP 27 or PACAP 38. VIP neuroprotective effects were lost in mice lacking VPAC2 receptor. In situ hybridization confirmed the presence of VPAC2 mRNA. These data suggest that, in this model, VIP‐induced neuroprotection is mediated by VPAC2 receptors. The pharmacology of this VPAC2 receptor seems unconventional as PACAP does not mimic VIP effects and PHI acts with a comparable potency.
ISSN:0077-8923
1749-6632
DOI:10.1196/annals.1317.071