PRECONDITIONING PROMOTES GABA- AND GLUTAMATERGIC NEURONS IN NEONATAL HYPOXICISCHEMIC BRAIN INJURY

BENITEZ, SERGIO; CASTRO, ANALÍA; ORTIZ MALDONADO, VALENTIN; SAVASTANO, LUIS; FITT MARCOS; SELTZER, ALICIA; MUÑOZ, ESTELA

San Juan

Congreso; SECOND JOINT MEETING OF THE BIOLOGY SOCIETIES FROM ARGENTINA; 2011

Hypoxic preconditioning (HC) protects from ischemic brain lesionsvia neurogenesis. GABAergic neurons are recognized by GAD1/GAD67.The differentiation factor NeuroD1/BETA2 acts as a hingeelement that favors differentiation of glutamatergic over GABAergicneurons. HC-induced neurogenesis may be mediated by both molecular determinants. We analyzed three groups: control (C: shamoperated non-asphyxiated P8 pups), lesioned (L: P8 pups with permanent ligation of the right carotid artery followed by hypoxia),and preconditioned and lesioned (PCL: P7 pups in auto-hypoxicenvironment before injury). Samples were collected at P15. Thehippocampal and cerebellar expression of both markers was evaluated by IHQ and WB. The PCL group showed an increase inGABAergic neurons near the granular layer of the dentate gyrusand in the cerebellar Purkinje cell layer. In the L group, NeuroD1-positive cells decreased in the hippocampal dentate gyrus, cerebellar external germinal and internal granular layers. Migrating immunoreactive cells decreased in the same brain areas. WB confirmedthese results. These observations indicate that both cellular phenotypes are induced by HC.