| Literature DB >> 21524251 |
Sandrine Passemard1, Paulina Sokolowska, Leslie Schwendimann, Pierre Gressens.
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.Entities:
Mesh:
Substances:
Year: 2011 PMID: 21524251 PMCID: PMC3370262 DOI: 10.2174/138161211795589409
Source DB: PubMed Journal: Curr Pharm Des ISSN: 1381-6128 Impact factor: 3.116