Prenatal ethanol exposure and cerebellar development in rats

Nathaniel, E.J.H.; Nathaniel, Doris R.; Mohamed, Seham M.; Nathaniel, L.; Kowalzik, C.; Nahnybida, L.

doi:10.1016/0014-4886(86)90179-2

Cited by 31 publications

(4 citation statements)

References 11 publications

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“…This is of particular interest because the cerebellum may be particularly vulnerable to the effects of early alcohol exposure. For example, perinatal alcohol exposure has been shown to decrease cerebellar weight and volume (Maier et al., 1997, 1999b; Nathaniel et al., 1986a,b; Weinberg, 1985), reduce cerebellar Purkinje and granule cell number and density (Bonthius and West, 1990, 1991; Maier and West, 2001; Maier et al., 1999b; McGoey et al., 2003), and generally reduced expression of neurotrophin receptors in the cerebellum (Moore et al., 2004). Children with FAS also show reductions in the size of the cerebellum (Mattson et al., 1996; O’Hare et al., 2005; Sowell et al., 1996, 2001a,b, 2002).…”

Section: Discussionmentioning

confidence: 99%

Environmental Enrichment Alters Neurotrophin Levels After Fetal Alcohol Exposure in Rats

Parks¹,

McMechan²,

Hannigan³

et al. 2008

Alcoholism Clin & Exp Res

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Background Prenatal alcohol exposure causes abnormal brain development, leading to behavioral deficits, some of which can be ameliorated by environmental enrichment. As both environmental enrichment and prenatal alcohol exposure can individually alter neurotrophin expression, we studied the interaction of prenatal alcohol and postweaning environmental enrichment on brain neurotrophin levels in rats. Methods Pregnant rats received alcohol by gavage, 0, 4, or 6 g / kg / d (Zero, Low, or High groups), or no treatment (Naïve group), on gestational days 8 to 20. After weaning on postnatal day 21, offspring were housed for 6 weeks in Isolated, Social, or Enriched conditions. Levels of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), and neurotrophin-3 (NT-3) were then measured in frontal cortex, occipital cortex, hippocampus, and cerebellar vermis. Results Prenatal alcohol exposure increased NGF levels in frontal cortex (High-dose group) and cerebellar vermis (High- and Low-dose groups); increased BDNF in frontal cortex, occipital cortex and hippocampus (Low-dose groups), and increased NT-3 in hippocampus and cerebellar vermis (High-dose). Environmental enrichment resulted in lower NGF, BDNF, and NT-3 levels in occipital cortex and lower NGF in frontal cortex. The only significant interaction between prenatal alcohol treatment and environment was in cerebellar vermis where NT-3 levels were higher for enriched animals after prenatal alcohol exposure, but not for animals housed under Isolated or Social conditions. Conclusions Both prenatal alcohol exposure and postweaning housing conditions alter brain neurotrophin levels, but the effects appear to be largely independent. Although environmental enrichment can improve functional outcomes, these results do not provide strong support for the hypothesis that rearing in a complex environment ameliorates prenatal alcohol effects on brain neurotrophin levels in rats.

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Section: Discussionmentioning

confidence: 99%

Environmental Enrichment Alters Neurotrophin Levels After Fetal Alcohol Exposure in Rats

Parks¹,

McMechan²,

Hannigan³

et al. 2008

Alcoholism Clin & Exp Res

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“…While profound cerebellar cell losses are seen following exposure during the early neonatal period (e.g., Hamre and West, 1993), prenatal exposure does produce a variety of effects. These include overall reduction of cerebellar mass (Nathaniel et al, 1986), significant reductions in Purkinje cell neurofilament protein and dendritic extension, reflecting delayed maturation (Poltorak et al, 1990), and delayed maturation of Bergmann glia, coincident with retarded granule cell migration (Shetty and Phillips, 1992). Certain of the alterations in NTF receptor expression could contribute to these and other abnormalities: TrkC, for example, which was decreased in this region, is important for Purkinje cell maturation during these periods (Davies, 1994).…”

Section: Regional Patterns Of Receptor Modificationmentioning

confidence: 94%

Ethanol exposure alters neurotrophin receptor expression in the rat central nervous system: Effects of prenatal exposure

et al. 2004

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Developmental ethanol exposure produces significant central nervous system (CNS) abnormalities. The cellular mechanisms of ethanol neurotoxicity, however, remain elusive. Recent data implicate altered neurotrophin signaling pathways in ethanol-mediated neuronal death. The present study investigated ethanol-induced alterations in neurotrophin receptor proteins in the rat CNS following chronic ethanol treatment during gestation, via liquid diet to pregnant dams. Brains were dissected on P1 and P10, and Western blots for the neurotrophin receptors TrkA, TrkB, TrkC, and p75 were quantified. Such ethanol treatment produced significant changes in neurotrophin receptor levels in the hippocampus, septum, cerebral cortex, and cerebellum. Receptor levels in hippocampus, septum, and cerebellum, tended to be decreased, while levels in cortex were consistently increased. Males were generally more affected than females. While most of these alterations were transient, sustained or delayed changes were present in P10 septum, cortex, and cerebellum. These results indicate that developmental ethanol exposure produces major changes in the normal physiological levels of the neurotrophin receptors throughout the CNS. These changes in the receptor complement during critical prenatal stages could relate to the anomalous development of the CNS seen in the fetal alcohol syndrome. This relationship is discussed, together with the potential biological effects of such dramatic changes in neurotrophin receptor expression.

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“…Numerous studies in the adult animal have shown that the cerebellum is very sensitive to ethanol. 28,29,35,36 In the chick, the cerebellum develops from the two separate lateral plates which meet and fuse in the midline on embryonic day 8 (E8). Granule cerebellar progenitor cells arise from the rhombic lip of each cerebellar plate.…”

mentioning

confidence: 99%

Maturation of cerebellar granule cells is delayed in cultures derived from ethanol‐treated chick embryos: Survival and proliferation studies

Srivastava

Vernadakis

1995

Intl J of Devlp Neuroscience

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Previous studies from this laboratory have shown that ethanol administration to chick embryos during embryonic days 1-3, a critical period of neuroembryogenesis, differentially affects primordial CNS structures. In this study, chick embryos were treated in ovo with ethanol (10 mg/50 microliter/day) at E1 to E3. At 14 days of embryonic age cerebellar (E14CE) granule cell cultures were prepared from both control and ethanol-treated embryos. Growth patterns were evaluated morphologically and the neuronal nature of these cultures was evaluated immunocytochemically. E14CE granule cell cultures exhibited neurofilament immunoreactivity demonstrating the neuronal-nature of these cultures. In addition E14CE granule cultures contained numerous glutamatergic neurons as assessed by positive glutamate immunoreactivity and also some GABAergic neurons as assessed by positive GABA immunoreactivity. Cultures derived from both control and ethanol-treated embryos were labeled with 3H-thymidine and assessed for effects on survival and proliferation in culture. Cultures derived from ethanol-treated embryos showed a higher rate of proliferation and survival during the first 3 days in culture as compared to those derived from controls. However, after 3 days in culture, survival was lower in the cultures from ethanol-treated embryos as compared to those derived from controls. We interpret these findings to mean that (a) ethanol arrested cerebellar granule cell development at an immature state; (b) immature neurons have a higher survival capacity than differentiated neurons; and (c) ethanol accelerates normal neuronal cell death as previously reported.

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Prenatal ethanol exposure and cerebellar development in rats

Cited by 31 publications

References 11 publications

Environmental Enrichment Alters Neurotrophin Levels After Fetal Alcohol Exposure in Rats

Environmental Enrichment Alters Neurotrophin Levels After Fetal Alcohol Exposure in Rats

Ethanol exposure alters neurotrophin receptor expression in the rat central nervous system: Effects of prenatal exposure

Maturation of cerebellar granule cells is delayed in cultures derived from ethanol‐treated chick embryos: Survival and proliferation studies

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