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Among the consequences of excessive activation of the <jats:italic>N<\/jats:italic>\u2010methyl\u2010<jats:sc>d<\/jats:sc>\u2010aspartate (<jats:styled-content style=\"fixed-case\">NMDA<\/jats:styled-content>)\u2010type glutamate are oxidative stress caused by free radical release from damaged mitochondria, neuronal death and subsequent loss of connectivity. Drugs that could protect nervous tissue and support regeneration are attractive therapeutic options. The hepatocarcinoma intestine pancreas protein\/pancreatitis\u2010associated protein I (<jats:styled-content style=\"fixed-case\">HIP<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">PAP<\/jats:styled-content>) or Reg3<jats:italic>\u03b1<\/jats:italic>, which is approved for clinical testing for the protection and regeneration of the liver, is upregulated in the central nervous system following injury or disease. Here, we examined the neuroprotective\/neuroregenerative potential of <jats:styled-content style=\"fixed-case\">HIP<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">PAP<\/jats:styled-content> following excitotoxic brain injury.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We studied the expression of HIP\/PAP and two of its putative effectors, <jats:styled-content style=\"fixed-case\">cAMP<\/jats:styled-content>\u2010regulated phosphoprotein 19 (ARPP19) and growth\u2010associated protein 43 (GAP\u201043), in the neonatal brain, and the protective\/regenerative properties of HIP\/PAP in three paradigms of perinatal excitotoxicity: intracerebral injection of the NMDA agonist ibotenate in newborn pups, a pediatric model of traumatic brain injury, and cultured primary cortical neurons.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">HIP<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">PAP<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> ARPP<\/jats:styled-content>19, and <jats:styled-content style=\"fixed-case\">GAP<\/jats:styled-content>\u201043 were expressed in the neonatal mouse brain. <jats:styled-content style=\"fixed-case\">HIP<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">PAP<\/jats:styled-content> prevented the formation of cortical and white matter lesions and reduced neuronal death and glial activation following excitotoxic insults in vivo. In vitro, <jats:styled-content style=\"fixed-case\">HIP<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">PAP<\/jats:styled-content> promoted neuronal survival, preserved neurite complexity and fasciculation, and protected cell contents from reactive oxygen species (<jats:styled-content style=\"fixed-case\">ROS<\/jats:styled-content>)\u2010induced damage.<\/jats:p><\/jats:sec><jats:sec><jats:title>Interpretation<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">HIP<\/jats:styled-content>\/<jats:styled-content style=\"fixed-case\">PAP<\/jats:styled-content> has strong neuroprotective\/neuroregenerative potential following excitotoxic injury to the developing brain, and could represent an interesting therapeutic strategy in perinatal brain injury.<\/jats:p><\/jats:sec>","DOI":"10.1002\/acn3.127","type":"journal-article","created":{"date-parts":[[2014,10,9]],"date-time":"2014-10-09T05:12:02Z","timestamp":1412831522000},"page":"739-754","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":31,"title":["HIP\/PAP prevents excitotoxic neuronal death and promotes plasticity"],"prefix":"10.1002","volume":"1","author":[{"given":"Parthiv","family":"Haldipur","sequence":"first","affiliation":[{"name":"National Brain Research Centre Manesar India"},{"name":"Centre for Neuroscience IISC Bangalore India"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nina","family":"Dupuis","sequence":"additional","affiliation":[{"name":"Inserm U1141 Paris France"},{"name":"Univ Paris Diderot Sorbonne Paris Cit\u00e9 UMRS 1141 Paris France"},{"name":"PremUP Paris 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