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Current Pharmaceutical Design

Editor-in-Chief

ISSN (Print): 1381-6128
ISSN (Online): 1873-4286

VIP-induced Neuroprotection of the Developing Brain

Author(s): Sandrine Passemard, Paulina Sokolowska, Leslie Schwendimann and Pierre Gressens

Volume 17, Issue 10, 2011

Page: [1036 - 1039] Pages: 4

DOI: 10.2174/138161211795589409

Price: $65

Abstract

Excitotoxicity is a key molecular mechanism of perinatal brain damage and is associated with cerebral palsy and long term cognitive deficits. VIP induces a potent neuroprotection against perinatal excitotoxic white matter damage. VIP does not prevent the initial appearance of white matter lesion but promotes a secondary repair with axonal regrowth. This plasticity mechanism involves an atypical VPAC2 receptor and BDNF production. Stable VIP agonists mimic VIP effects when given systemically and exhibit a large therapeutic window. Unraveling cellular and molecular targets of VIP effects against perinatal white matter lesions could provide a more general rationale to understand the neuroprotection of the developing white matter against excitotoxic insults.

Keywords: Neuroprotection, cerebral palsy, plasticity, preterm infant, VPAC receptor, NAP, excitotoxicity, perinatal, multifactorial, ionotropic, phosphoinositide, cytoarchitectonic, astrocytic, murine, dysgeneses, isoleucine, forskolin, calmodulin, heterodimers, endopeptidases, methionine


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