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Volume 17, Issue 10
  • ISSN: 1381-6128
  • E-ISSN: 1873-4286

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.

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/content/journals/cpd/10.2174/138161211795589409
2011-04-01
2025-05-06

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  • Article Type:     Research Article
Keyword(s): astrocytic; calmodulin; cerebral palsy; cytoarchitectonic; dysgeneses; endopeptidases; excitotoxicity; forskolin; heterodimers; ionotropic; isoleucine; methionine; multifactorial; murine; NAP; Neuroprotection; perinatal; phosphoinositide; plasticity; preterm infant; VPAC receptor

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