zma000467 Abstract Herrera-Marschitz Herrera-Marschitz Mario M Prof. Dr.

University of Chile, Medical Faculty, Programm of Molecular & Clinical Pharmacology, ICBM, Santiago 7, P.O. Box 70.000, ChileUniversity of Chile, Medical Faculty, Programm of Molecular & Clinical Pharmacology, ICBM, Santiago, Chile

mh-marschitz@med.uchile.cl author Golubnitchaja Golubnitchaja Olga O Prof. Dr.

University of Bonn, Dept. of Experimental Radiology, Bonn, Germany

olga.golubnitschaja@ukb.uni-bonn.de author Bustamante Bustamante Diego D Prof.

University of Chile, Medical Faculty, Programm of Molecular & Clinical Pharmacology, ICBM, Santiago, Chile

dbustama@med.uchile.cl author Morales Morales Paola P Prof.

University of Chile, Medical Faculty, Programm of Molecular & Clinical Pharmacology, ICBM, Santiago, Chile

pmorales@med.uchile.cl author Klawitter Klawitter Verena V Prof.

University of Chile, Medical Faculty, Programm of Molecular & Clinical Pharmacology, ICBM, Santiago, Chile

vklawitter@med.uchile.cl author Fiedler Fiedler Jenny L. JL Prof. Ass.

University of Chile, Chemical and Pharmaceutical Sciences Faculty, Department of Biochemistry and Molecular Biology, Laboratory of Neurobiochemistry, Santiago, Chile

jfiedler@ciq.uchile.cl author Morelli Morelli Micaela M Dr.

University of Cagliari, Dept. Toxicology, Cagliari, Italy

morelli@unica.it author Tasker Tasker Andrew A Prof. Dr.

University of Prince Edward Island, Department of biomedical Sciences, Charlottetown, Canada

tasker@upei.ca author Gomez-Urquijo Gomez-Urquijo Sonia S Dr.

University of the Basque Country, Faculty of Medicine, Department of Neuroscience, Spain

soniam.gomez@ehu.es author Hökfelt Hökfelt Tomas T Prof. Dr.

Karolinska Institutet, Department of Neuroscience, Stockholm, Schweden

tomas.hokfelt@ki.se author Goiny Goiny Michel M PhD.

Karolinska Institutet, Dept. of Physiology & Pharmacology, Stockholm, Schweden

goiny.michel@ki.se author German Medical Science GMS Publishing House

Düsseldorf

610 Special areas 20070925 20070925 20071001 20071114 engl 1860-3572 24 4 GMS Zeitschrift für Medizinische Ausbildung GMS Z Med Ausbild 173 Interruption of oxygen availability and re-oxygenation at birth implies a severe metabolic insult, affecting the development of the central nervous system (CNS), increasing its vulnerability to challenges occurring at adult stages. It has been reported that perinatal asphyxia produces regionally specific neuronal decrease and neurite atrophy in basal ganglia, and hippocampus. In hippocampus, a concomitant increase of neurogenesis and neurite hypertrophy has also been observed. The potential neuroprotection of nicotinamide, a non-selective inhibitor of poly (ADP-ribose) polymerase (PARP-1), has been investigated, finding functional and morphological improvements when administered 24h after the insult (0.8 mmol/kg, i.p., 24, 48 and 72 h after birth.). The main effect of nicotinamide has been seen in neostriatum, preventing an asphyxia-induced decrease of the number of nNOS cells, and nNOS- and dopamine-like neurite atrophy. The present results support the idea that nicotinamide can prevent the effects elicited by a sustained energy-failure condition, as occurring during perinatal asphyxia, enlightening the enzyme PARP-1 as a novel target for neuronal protection. The support by FONDECYT, ICBM-Enlace, DAAD-CONICYT Programme-2007 grants is acknowledged. Abstract Interruption of oxygen availability and re-oxygenation at birth implies a severe metabolic insult, affecting the development of the central nervous system (CNS), increasing its vulnerability to challenges occurring at adult stages. It has been reported that perinatal asphyxia produces regionally specific neuronal decrease and neurite atrophy in basal ganglia, and hippocampus. In hippocampus, a concomitant increase of neurogenesis and neurite hypertrophy has also been observed. The potential neuroprotection of nicotinamide, a non-selective inhibitor of poly (ADP-ribose) polymerase (PARP-1), has been investigated, finding functional and morphological improvements when administered 24h after the insult (0.8 mmol/kg, i.p., 24, 48 and 72 h after birth.). The main effect of nicotinamide has been seen in neostriatum, preventing an asphyxia-induced decrease of the number of nNOS cells, and nNOS- and dopamine-like neurite atrophy. The present results support the idea that nicotinamide can prevent the effects elicited by a sustained energy-failure condition, as occurring during perinatal asphyxia, enlightening the enzyme PARP-1 as a novel target for neuronal protection. The support by FONDECYT, ICBM-Enlace, DAAD-CONICYT Programme-2007 grants is acknowledged. 0 0 0 0