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Mechanisms of VIP‐Induced Neuroprotection against Neonatal Excitotoxicity
Author(s) -
RANGON CLAIREMARIE,
DICOU ELENI,
GOURSAUD STÉPHANIE,
MOUNIEN LOURDES,
JÉGOU SYLVIE,
JANET THIERRY,
MULLER JEANMARC,
LELIÈVRE VINCENT,
GRESSENS PIERRE
Publication year - 2006
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1317.071
Subject(s) - neuroprotection , vasoactive intestinal peptide , receptor , excitotoxicity , adenylate kinase , pituitary adenylate cyclase activating peptide , pharmacology , chemistry , neuropeptide , biology , biochemistry , glutamate receptor
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.