Sandrine Passemard, Paulina Sokolowska, Leslie Schwendimann and Pierre Gressens Pages 1036 - 1039 ( 4 )
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.
Neuroprotection,cerebral palsy,plasticity,preterm infant,VPAC receptor,NAP,excitotoxicity,perinatal,multifactorial,ionotropic,phosphoinositide,cytoarchitectonic,astrocytic,murine,dysgeneses,isoleucine,forskolin,calmodulin,heterodimers,endopeptidases,methionine
, , , Inserm U 676, Hopital Robert Debre, 48 Blvd Serurier, 75019 Paris, France.