Talk:Neural - Cerebellum Development: Difference between revisions

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PMID 21858122
PMID 21858122
===Alcohol exposure decreases CREB binding protein expression and histone acetylation in the developing cerebellum===
PLoS One. 2011;6(5):e19351. Epub 2011 May 31.
Guo W, Crossey EL, Zhang L, Zucca S, George OL, Valenzuela CF, Zhao X.
Source
Department of Neurosciences, University of New Mexico School of Medicine, Albuquerque, New Mexico, United States of America.
Abstract
BACKGROUND:
Fetal alcohol exposure affects 1 in 100 children making it the leading cause of mental retardation in the US. It has long been known that alcohol affects cerebellum development and function. However, the underlying molecular mechanism is unclear.
METHODOLOGY/PRINCIPAL FINDINGS:
We demonstrate that CREB binding protein (CBP) is widely expressed in granule and Purkinje neurons of the developing cerebellar cortex of naïve rats. We also show that exposure to ethanol during the 3(rd) trimester-equivalent of human pregnancy reduces CBP levels. CBP is a histone acetyltransferase, a component of the epigenetic mechanism controlling neuronal gene expression. We further demonstrate that the acetylation of both histone H3 and H4 is reduced in the cerebellum of ethanol-treated rats.
CONCLUSIONS/SIGNIFICANCE:
These findings indicate that ethanol exposure decreases the expression and function of CBP in the developing cerebellum. This effect of ethanol may be responsible for the motor coordination deficits that characterize fetal alcohol spectrum disorders.
PMID 21655322

Revision as of 23:50, 22 September 2011

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Cite this page: Hill, M.A. (2024, May 8) Embryology Neural - Cerebellum Development. Retrieved from https://embryology.med.unsw.edu.au/embryology/index.php/Talk:Neural_-_Cerebellum_Development

2011

Preterm delivery disrupts the developmental program of the cerebellum

PLoS One. 2011;6(8):e23449. Epub 2011 Aug 17.

Haldipur P, Bharti U, Alberti C, Sarkar C, Gulati G, Iyengar S, Gressens P, Mani S. Source National Brain Research Centre, Manesar, Haryana, India.

Abstract

A rapid growth in human cerebellar development occurs in the third trimester, which is impeded by preterm delivery. The goal of this study was to characterize the impact of preterm delivery on the developmental program of the human cerebellum. Still born infants, which meant that all development up to that age had taken place in-utero, were age paired with preterm delivery infants, who had survived in an ex-utero environment, which meant that their development had also taken place outside the uterus. The two groups were assessed on quantitative measures that included molecular markers of granule neuron, purkinje neuron and bergmann glia differentiation, as well as the expression of the sonic hedgehog signaling pathway, that is important for cerebellar growth. We report that premature birth and development in an ex-utero environment leads to a significant decrease in the thickness and an increase in the packing density of the cells within the external granular layer and the inner granular layer well, as a reduction in the density of bergmann glial fibres. In addition, this also leads to a reduced expression of sonic hedgehog in the purkinje layer. We conclude that the developmental program of the cerebellum is specifically modified by events that follow preterm delivery.

PMID 21858122

Alcohol exposure decreases CREB binding protein expression and histone acetylation in the developing cerebellum

PLoS One. 2011;6(5):e19351. Epub 2011 May 31.

Guo W, Crossey EL, Zhang L, Zucca S, George OL, Valenzuela CF, Zhao X. Source Department of Neurosciences, University of New Mexico School of Medicine, Albuquerque, New Mexico, United States of America.

Abstract

BACKGROUND: Fetal alcohol exposure affects 1 in 100 children making it the leading cause of mental retardation in the US. It has long been known that alcohol affects cerebellum development and function. However, the underlying molecular mechanism is unclear.

METHODOLOGY/PRINCIPAL FINDINGS: We demonstrate that CREB binding protein (CBP) is widely expressed in granule and Purkinje neurons of the developing cerebellar cortex of naïve rats. We also show that exposure to ethanol during the 3(rd) trimester-equivalent of human pregnancy reduces CBP levels. CBP is a histone acetyltransferase, a component of the epigenetic mechanism controlling neuronal gene expression. We further demonstrate that the acetylation of both histone H3 and H4 is reduced in the cerebellum of ethanol-treated rats.

CONCLUSIONS/SIGNIFICANCE: These findings indicate that ethanol exposure decreases the expression and function of CBP in the developing cerebellum. This effect of ethanol may be responsible for the motor coordination deficits that characterize fetal alcohol spectrum disorders.

PMID 21655322