IBCN   20355
INSTITUTO DE BIOLOGIA CELULAR Y NEUROCIENCIA "PROFESOR EDUARDO DE ROBERTIS"
Unidad Ejecutora - UE
artículos
Título:
PRENATAL ETHANOL EXPOSURE REDUCES THE EXPRESSION OF THE TRANSCRIPTIONAL FACTOR PAX6 IN THE DEVELOPING RAT BRAIN
Autor/es:
ARONNE MP. EVRARD SG. MIROCHNIC S, BRUSCO A
Revista:
Annals of the New Your Academy of Sciences
Editorial:
Blackwell Publishing o behalf of the New York Academy of Sciences
Referencias:
Lugar: Boston, Masachusset, USA; Año: 2008 vol. 1139 p. 478 - 498
ISSN:
0077-8923
Resumen:
Prenatal ethanol exposure (PEE) induces functional and structural disorders in the
developing central nervous system (CNS). The relationship between radial glial cells
(RGCs) and migrating neuroblasts is crucial for the establishment of normal CNS laminated
structures. Pax6, a transcription factor involved in mammalian neuronal developmental
processes, could be affected by PEE, as it is already known to occur in
amphibians. From gestational day 10 to 18 (G10-G18), pregnant Wistar rats were subjected
to an intraperitoneal injection of a daily ethanol (EtOH) 3.5 g/kg dose. Control
pregnant rats received equivalent volumes of saline solution. Fetal weights and cerebral
cortex thickness were significantly lower in G18 PEE than in control fetuses, and neural
tube defects were found in the G18 PEE fetuses. Cortical expression of vimentin (an
RGC cytoskeletal marker), S-100b protein (a neurotrophic factor and cytosolic marker
of RGCs during embryonic development), and 68 kDa neurofilaments (a neuronal cytoskeletal
marker) were also decreased in G18 PEE fetuses. At G14, a reduction in Pax6
processes, could be affected by PEE, as it is already known to occur in
amphibians. From gestational day 10 to 18 (G10-G18), pregnant Wistar rats were subjected
to an intraperitoneal injection of a daily ethanol (EtOH) 3.5 g/kg dose. Control
pregnant rats received equivalent volumes of saline solution. Fetal weights and cerebral
cortex thickness were significantly lower in G18 PEE than in control fetuses, and neural
tube defects were found in the G18 PEE fetuses. Cortical expression of vimentin (an
RGC cytoskeletal marker), S-100b protein (a neurotrophic factor and cytosolic marker
of RGCs during embryonic development), and 68 kDa neurofilaments (a neuronal cytoskeletal
marker) were also decreased in G18 PEE fetuses. At G14, a reduction in Pax6
processes, could be affected by PEE, as it is already known to occur in
amphibians. From gestational day 10 to 18 (G10-G18), pregnant Wistar rats were subjected
to an intraperitoneal injection of a daily ethanol (EtOH) 3.5 g/kg dose. Control
pregnant rats received equivalent volumes of saline solution. Fetal weights and cerebral
cortex thickness were significantly lower in G18 PEE than in control fetuses, and neural
tube defects were found in the G18 PEE fetuses. Cortical expression of vimentin (an
RGC cytoskeletal marker), S-100b protein (a neurotrophic factor and cytosolic marker
of RGCs during embryonic development), and 68 kDa neurofilaments (a neuronal cytoskeletal
marker) were also decreased in G18 PEE fetuses. At G14, a reduction in Pax6
Pax6, a transcription factor involved in mammalian neuronal developmental
processes, could be affected by PEE, as it is already known to occur in
amphibians. From gestational day 10 to 18 (G10-G18), pregnant Wistar rats were subjected
to an intraperitoneal injection of a daily ethanol (EtOH) 3.5 g/kg dose. Control
pregnant rats received equivalent volumes of saline solution. Fetal weights and cerebral
cortex thickness were significantly lower in G18 PEE than in control fetuses, and neural
tube defects were found in the G18 PEE fetuses. Cortical expression of vimentin (an
RGC cytoskeletal marker), S-100b protein (a neurotrophic factor and cytosolic marker
of RGCs during embryonic development), and 68 kDa neurofilaments (a neuronal cytoskeletal
marker) were also decreased in G18 PEE fetuses. At G14, a reduction in Pax6Pax6
cortical expression was found. Our results suggest that PEE reduces Pax6 expression
in undifferentiated mammalian CNS cells. This could be one of the factors that induce
RGCs and neuronal alterations at end-gestation. These alterations could be involved in
the pathophysiology of neurodevelopmental disorders observed in the children affected
by the fetal alcohol syndrome.
in undifferentiated mammalian CNS cells. This could be one of the factors that induce
RGCs and neuronal alterations at end-gestation. These alterations could be involved in
the pathophysiology of neurodevelopmental disorders observed in the children affected
by the fetal alcohol syndrome.
in undifferentiated mammalian CNS cells. This could be one of the factors that induce
RGCs and neuronal alterations at end-gestation. These alterations could be involved in
the pathophysiology of neurodevelopmental disorders observed in the children affected
by the fetal alcohol syndrome.
Pax6 expression
in undifferentiated mammalian CNS cells. This could be one of the factors that induce
RGCs and neuronal alterations at end-gestation. These alterations could be involved in
the pathophysiology of neurodevelopmental disorders observed in the children affected
by the fetal alcohol syndrome.