Altered Purkinje cell maturation in rats exposed prenatally to ethanol

Mohamed, Seham M.; Nathaniel, E.J.H.; Nathaniel, Doris R.; Snell, Linda

doi:10.1016/0014-4886(87)90280-9

Cited by 26 publications

(2 citation statements)

References 20 publications

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“…Its genesis is completed before birth whereas their maturation is a postnatal event (Altman, 1969, 1972). At 7 days, the Purkinje cells in the rat form a closely packed single row of cells below the molecular layer (Mohammed et al, 1987). Cells of the internal granular layer in mice and rats are developed from the migrating cells of the external granular layer (Marcelo and Fahad, 2002).…”

Section: Introductionmentioning

confidence: 99%

The development of sensorimotor reflexes in albino mice; albino rats and black‐hooded rats

Allam

Abo‐Eleneen

2012

Intl J of Devlp Neuroscience

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The present investigation aimed to show the differences in the development of sensorimotor reflexes and their relationship to the structural changes in spinal cord, cerebellum and cerebral cortex in three rodent species. The three species are albino rats (A-Rats), black-hooded rats (B-Rats) and albino mice. The development of selected reflexes was examined from day (D1) to D21. The structural changes were investigated at D7, D14, and D21. The following reflexes were analyzed: fore-limb/hind-limb grasp, surface body righting, fore-limb hopping, chin tactile placing, visual placing and body righting in the air. The developmental pattern of the reflexes was different in three rodent species. Although the black-hooded rats and albino rats belong to the same species, they are different in their appearance and developmental pattern. The development of external features and sensorimotor reflexes appeared earlier in mice than in A-Rats and B-Rats. At D7, differentiation of neurons was observed in the spinal cord while in cerebellum and cerebrum the neurons were found to be undifferentiated. At D14 and D21, the differentiated neurons were observed in spinal cord, cerebellum and cerebrum. Our data indicate that the developmental pattern of the reflexes in rodents may not be species specific but may be related to the animal strain.

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Section: Introductionmentioning

confidence: 99%

The development of sensorimotor reflexes in albino mice; albino rats and black‐hooded rats

Allam

Abo‐Eleneen

2012

Intl J of Devlp Neuroscience

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“…PTEN expression and activity were also examined, because PTEN dephosphorylates and negatively regulates PI3 kinase function (38), and the effects of ethanol on phosphatase and tensin homolog deleted in chromosome 10 (PTEN) were unknown. Cerebellar tissue was studied, because it represents a major in vivo target of ethanol neurotoxicity (2,39).…”

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confidence: 99%

Ethanol Impairs Insulin-stimulated Neuronal Survival in the Developing Brain

Yeon

Chang

et al. 2003

Journal of Biological Chemistry

129

166

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Gestational exposure to ethanol causes fetal alcohol syndrome, which is associated with cerebellar hypoplasia. Previous in vitro studies demonstrated ethanol-impaired neuronal survival with reduced signaling through the insulin receptor (IR␤). We examined insulin signaling in an experimental rat model of chronic gestational exposure to ethanol in which the pups exhibited striking cerebellar hypoplasia with increased apoptosis. Immunoprecipitation and Western blot analyses detected reduced levels of tyrosyl-phosphorylated IR␤, tyrosyl-phosphorylated insulin receptor substrate-1 (IRS-1), and p85-associated IRS-1 but no alterations in IR␤, IRS-1, or p85 protein expression in cerebellar tissue from ethanol-exposed pups. In addition, ethanol exposure significantly reduced the levels of total phosphoinositol 3-kinase, Akt kinase, phospho-BAD (inactive), and glyceraldehyde-3-phosphate dehydrogenase and increased the levels of glycogen synthase kinase-3 activity, activated BAD, phosphatase and tensin homolog deleted in chromosome 10 (PTEN) protein, and PTEN phosphatase activity in cerebellar tissue. Cerebellar neurons isolated from ethanol-exposed pups had reduced levels of insulin-stimulated phosphoinositol 3-kinase and Akt kinase activities and reduced insulin inhibition of PTEN and glycogen synthase kinase-3 activity. The results demonstrate that cerebellar hypoplasia produced by chronic gestational exposure to ethanol is associated with impaired survival signaling through insulin-regulated pathways, including failure to suppress PTEN function.Ethanol exposure during development is one of the leading causes of mental retardation in Europe and North America. Heavy gestational exposure to ethanol can cause fetal alcohol syndrome, which encompasses a broad array of neurologic and systemic lesions including central nervous system (CNS) malformations such as microencephaly, reduced cerebral white matter volume, ventriculomegaly, cerebellar hypoplasia, and disorders of neuronal migration (1). Experimental models of fetal alcohol syndrome have demonstrated that the accompanying CNS abnormalities are associated with impaired neuronal survival, growth, synaptogenesis, maturation, neurotransmitter function, and intracellular adhesion (2-7). Even with shorter durations and lower levels of exposure, ethanol can be neurotoxic during development and substantially reduce the populations of CNS neurons (2).Previous experiments demonstrated that neuronal loss following ethanol exposure was mediated by apoptosis (8 -10) or mitochondrial dysfunction (10 -12), and recent studies correlated these adverse effects of ethanol to inhibition of growth factor-stimulated survival signaling (9, 11-13). In the developing CNS, insulin and insulin-like growth factor type 1 (IGF-1) 1 receptors are abundantly expressed (14 -16), and the corresponding growth factor-stimulated responses are critical mediators of neuronal growth, viability, energy metabolism, and synapse formation. Because insulin and IGF-1 signaling pathways are among the important tar...

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