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.