IHEM   20887
INSTITUTO DE HISTOLOGIA Y EMBRIOLOGIA DE MENDOZA DR. MARIO H. BURGOS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Effect of preconditioning on gabaergic cell populations in a rat model of neonatal hypoxic-ischemic injury
Autor/es:
BENITEZ SG; CASTRO AE; ORTIZ MALDONADO V; SAVASTANO LE; FITT MR; SELTZER AM; MUÑOZ EM
Lugar:
San Juan
Reunión:
Congreso; SECOND JOINT MEETING OF THE BIOLOGY SOCIETIES FROM ARGENTINA; 2011
Institución organizadora:
Soc. de Biología de Cuyo
Resumen:
BIOCELL 35(3),2011 Res. Nr0. 315 NQ13 pp A283 Hypoxic preconditioning (HC) protects from ischemic brain lesions via neurogenesis. GABAergic neurons are recognized by GAD1/ GAD67.The differentiation factor NeuroD1/BETA2 acts as a hinge element that favors differentiation of glutamatergic over GABAergic neurons. 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-hypoxic environment before injury). Samples were collected at P15. The hippocampal and cerebellar expression of both markers was evaluated by IHQ and WB. The PCL group showed an increase in GABAergic neurons near the granular layer of the dentate gyrus and 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 confirmed these results. These observations indicate that both cellular phenotypes are induced by HC. GAD67.The differentiation factor NeuroD1/BETA2 acts as a hinge element that favors differentiation of glutamatergic over GABAergic neurons. 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-hypoxic environment before injury). Samples were collected at P15. The hippocampal and cerebellar expression of both markers was evaluated by IHQ and WB. The PCL group showed an increase in GABAergic neurons near the granular layer of the dentate gyrus and 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 confirmed these results. These observations indicate that both cellular phenotypes are induced by HC. GAD67.The differentiation factor NeuroD1/BETA2 acts as a hinge element that favors differentiation of glutamatergic over GABAergic neurons. 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-hypoxic environment before injury). Samples were collected at P15. The hippocampal and cerebellar expression of both markers was evaluated by IHQ and WB. The PCL group showed an increase in GABAergic neurons near the granular layer of the dentate gyrus and 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 confirmed these results. These observations indicate that both cellular phenotypes are induced by HC. neurogenesis. GABAergic neurons are recognized by GAD1/ GAD67.The differentiation factor NeuroD1/BETA2 acts as a hinge element that favors differentiation of glutamatergic over GABAergic neurons. 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-hypoxic environment before injury). Samples were collected at P15. The hippocampal and cerebellar expression of both markers was evaluated by IHQ and WB. The PCL group showed an increase in GABAergic neurons near the granular layer of the dentate gyrus and 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 confirmed these results. These observations indicate that both cellular phenotypes are induced by HC.