INVESTIGADORES
PITOSSI Fernando Juan
artículos
Título:
Prenatal inflammation impairs adult neurogenesis and memory related behavior through persistent hippocampal TGFâ1 downregulation.
Autor/es:
MARIANA GRACIARENA; AMAICHA M DEPINO; FERNANDO J PITOSSI
Revista:
BRAIN BEHAVIOR AND IMMUNITY
Editorial:
ACADEMIC PRESS INC ELSEVIER SCIENCE
Referencias:
Año: 2010 vol. 24 p. 1301 - 1309
ISSN:
0889-1591
Resumen:
Prenatal exposure to inflammatory stimuli is known to influence adult brain function. In addition, adult
hippocampal neurogenesis is impaired by a local pro-inflammatory microenvironment. On this basis, we
hypothesized that a pro-inflammatory insult during gestation would have negative effects on adult neurogenesis
in the offspring. Pregnant Wistar rats received subcutaneous injections of lipopolysaccharide
(LPS; 0.5 mg/kg) or saline every other day from gestational day 14 to 20. The adult offspring prenatally
treated with LPS showed a decrease in the proliferating cells and the newborn neurons of the dentate
gyrus. Furthermore, prenatal LPS treatment impaired performance in the neurogenesis-dependent novel
object recognition test. Maternal care was impaired by prenatal LPS administration but did not contribute
to the effects of prenatal LPS on adult neurogenesis. Persistent microglial activation and downregulated
expression of transforming growth factor beta-1 (TGFb1) occurred specifically in the adult hippocampus
of animals treated prenatally with LPS. Importantly, chronic hippocampal TGFb1 overexpression restored
neurogenesis as well as recognition memory performance to control levels.
These findings demonstrate that prenatal inflammation triggered by LPS impairs adult neurogenesis
and recognition memory. Furthermore, we provide a model of reduced adult neurogenesis with long-lasting
defined alterations in the neurogenic niche. Finally, we show that the expression of a single cytokine
(TGFb1) in the hippocampus can restore adult neurogenesis and its related behavior, highlighting the role
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
neurogenesis as well as recognition memory performance to control levels.
These findings demonstrate that prenatal inflammation triggered by LPS impairs adult neurogenesis
and recognition memory. Furthermore, we provide a model of reduced adult neurogenesis with long-lasting
defined alterations in the neurogenic niche. Finally, we show that the expression of a single cytokine
(TGFb1) in the hippocampus can restore adult neurogenesis and its related behavior, highlighting the role
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
neurogenesis as well as recognition memory performance to control levels.
These findings demonstrate that prenatal inflammation triggered by LPS impairs adult neurogenesis
and recognition memory. Furthermore, we provide a model of reduced adult neurogenesis with long-lasting
defined alterations in the neurogenic niche. Finally, we show that the expression of a single cytokine
(TGFb1) in the hippocampus can restore adult neurogenesis and its related behavior, highlighting the role
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
neurogenesis as well as recognition memory performance to control levels.
These findings demonstrate that prenatal inflammation triggered by LPS impairs adult neurogenesis
and recognition memory. Furthermore, we provide a model of reduced adult neurogenesis with long-lasting
defined alterations in the neurogenic niche. Finally, we show that the expression of a single cytokine
(TGFb1) in the hippocampus can restore adult neurogenesis and its related behavior, highlighting the role
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
of animals treated prenatally with LPS. Importantly, chronic hippocampal TGFb1 overexpression restored
neurogenesis as well as recognition memory performance to control levels.
These findings demonstrate that prenatal inflammation triggered by LPS impairs adult neurogenesis
and recognition memory. Furthermore, we provide a model of reduced adult neurogenesis with long-lasting
defined alterations in the neurogenic niche. Finally, we show that the expression of a single cytokine
(TGFb1) in the hippocampus can restore adult neurogenesis and its related behavior, highlighting the role
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
neurogenesis as well as recognition memory performance to control levels.
These findings demonstrate that prenatal inflammation triggered by LPS impairs adult neurogenesis
and recognition memory. Furthermore, we provide a model of reduced adult neurogenesis with long-lasting
defined alterations in the neurogenic niche. Finally, we show that the expression of a single cytokine
(TGFb1) in the hippocampus can restore adult neurogenesis and its related behavior, highlighting the role
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
neurogenesis as well as recognition memory performance to control levels.
These findings demonstrate that prenatal inflammation triggered by LPS impairs adult neurogenesis
and recognition memory. Furthermore, we provide a model of reduced adult neurogenesis with long-lasting
defined alterations in the neurogenic niche. Finally, we show that the expression of a single cytokine
(TGFb1) in the hippocampus can restore adult neurogenesis and its related behavior, highlighting the role
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
neurogenesis as well as recognition memory performance to control levels.
These findings demonstrate that prenatal inflammation triggered by LPS impairs adult neurogenesis
and recognition memory. Furthermore, we provide a model of reduced adult neurogenesis with long-lasting
defined alterations in the neurogenic niche. Finally, we show that the expression of a single cytokine
(TGFb1) in the hippocampus can restore adult neurogenesis and its related behavior, highlighting the role
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
of animals treated prenatally with LPS. Importantly, chronic hippocampal TGFb1 overexpression restored
neurogenesis as well as recognition memory performance to control levels.
These findings demonstrate that prenatal inflammation triggered by LPS impairs adult neurogenesis
and recognition memory. Furthermore, we provide a model of reduced adult neurogenesis with long-lasting
defined alterations in the neurogenic niche. Finally, we show that the expression of a single cytokine
(TGFb1) in the hippocampus can restore adult neurogenesis and its related behavior, highlighting the role
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
neurogenesis as well as recognition memory performance to control levels.
These findings demonstrate that prenatal inflammation triggered by LPS impairs adult neurogenesis
and recognition memory. Furthermore, we provide a model of reduced adult neurogenesis with long-lasting
defined alterations in the neurogenic niche. Finally, we show that the expression of a single cytokine
(TGFb1) in the hippocampus can restore adult neurogenesis and its related behavior, highlighting the role
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
neurogenesis as well as recognition memory performance to control levels.
These findings demonstrate that prenatal inflammation triggered by LPS impairs adult neurogenesis
and recognition memory. Furthermore, we provide a model of reduced adult neurogenesis with long-lasting
defined alterations in the neurogenic niche. Finally, we show that the expression of a single cytokine
(TGFb1) in the hippocampus can restore adult neurogenesis and its related behavior, highlighting the role
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
neurogenesis as well as recognition memory performance to control levels.
These findings demonstrate that prenatal inflammation triggered by LPS impairs adult neurogenesis
and recognition memory. Furthermore, we provide a model of reduced adult neurogenesis with long-lasting
defined alterations in the neurogenic niche. Finally, we show that the expression of a single cytokine
(TGFb1) in the hippocampus can restore adult neurogenesis and its related behavior, highlighting the role
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
of animals treated prenatally with LPS. Importantly, chronic hippocampal TGFb1 overexpression restored
neurogenesis as well as recognition memory performance to control levels.
These findings demonstrate that prenatal inflammation triggered by LPS impairs adult neurogenesis
and recognition memory. Furthermore, we provide a model of reduced adult neurogenesis with long-lasting
defined alterations in the neurogenic niche. Finally, we show that the expression of a single cytokine
(TGFb1) in the hippocampus can restore adult neurogenesis and its related behavior, highlighting the role
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
neurogenesis as well as recognition memory performance to control levels.
These findings demonstrate that prenatal inflammation triggered by LPS impairs adult neurogenesis
and recognition memory. Furthermore, we provide a model of reduced adult neurogenesis with long-lasting
defined alterations in the neurogenic niche. Finally, we show that the expression of a single cytokine
(TGFb1) in the hippocampus can restore adult neurogenesis and its related behavior, highlighting the role
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
neurogenesis as well as recognition memory performance to control levels.
These findings demonstrate that prenatal inflammation triggered by LPS impairs adult neurogenesis
and recognition memory. Furthermore, we provide a model of reduced adult neurogenesis with long-lasting
defined alterations in the neurogenic niche. Finally, we show that the expression of a single cytokine
(TGFb1) in the hippocampus can restore adult neurogenesis and its related behavior, highlighting the role
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
neurogenesis as well as recognition memory performance to control levels.
These findings demonstrate that prenatal inflammation triggered by LPS impairs adult neurogenesis
and recognition memory. Furthermore, we provide a model of reduced adult neurogenesis with long-lasting
defined alterations in the neurogenic niche. Finally, we show that the expression of a single cytokine
(TGFb1) in the hippocampus can restore adult neurogenesis and its related behavior, highlighting the role
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
b1) occurred specifically in the adult hippocampus
of animals treated prenatally with LPS. Importantly, chronic hippocampal TGFb1 overexpression restored
neurogenesis as well as recognition memory performance to control levels.
These findings demonstrate that prenatal inflammation triggered by LPS impairs adult neurogenesis
and recognition memory. Furthermore, we provide a model of reduced adult neurogenesis with long-lasting
defined alterations in the neurogenic niche. Finally, we show that the expression of a single cytokine
(TGFb1) in the hippocampus can restore adult neurogenesis and its related behavior, highlighting the role
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
neurogenesis as well as recognition memory performance to control levels.
These findings demonstrate that prenatal inflammation triggered by LPS impairs adult neurogenesis
and recognition memory. Furthermore, we provide a model of reduced adult neurogenesis with long-lasting
defined alterations in the neurogenic niche. Finally, we show that the expression of a single cytokine
(TGFb1) in the hippocampus can restore adult neurogenesis and its related behavior, highlighting the role
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
neurogenesis as well as recognition memory performance to control levels.
These findings demonstrate that prenatal inflammation triggered by LPS impairs adult neurogenesis
and recognition memory. Furthermore, we provide a model of reduced adult neurogenesis with long-lasting
defined alterations in the neurogenic niche. Finally, we show that the expression of a single cytokine
(TGFb1) in the hippocampus can restore adult neurogenesis and its related behavior, highlighting the role
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
neurogenesis as well as recognition memory performance to control levels.
These findings demonstrate that prenatal inflammation triggered by LPS impairs adult neurogenesis
and recognition memory. Furthermore, we provide a model of reduced adult neurogenesis with long-lasting
defined alterations in the neurogenic niche. Finally, we show that the expression of a single cytokine
(TGFb1) in the hippocampus can restore adult neurogenesis and its related behavior, highlighting the role
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
b1 overexpression restored
neurogenesis as well as recognition memory performance to control levels.
These findings demonstrate that prenatal inflammation triggered by LPS impairs adult neurogenesis
and recognition memory. Furthermore, we provide a model of reduced adult neurogenesis with long-lasting
defined alterations in the neurogenic niche. Finally, we show that the expression of a single cytokine
(TGFb1) in the hippocampus can restore adult neurogenesis and its related behavior, highlighting the role
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
of TGFb1 in these processes.
b1) in the hippocampus can restore adult neurogenesis and its related behavior, highlighting the role
of TGFb1 in these processes.b1 in these processes.
