VIP-induced Neuroprotection of the Developing Brain

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

Journal Name: Current Pharmaceutical Design

Volume 17 , Issue 10 , 2011

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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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Article Details

Year: 2011
Published on: 01 March, 2012
Page: [1036 - 1039]
Pages: 4
DOI: 10.2174/138161211795589409
Price: $65

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