Neuronal plasticity in the developing chick brain: interaction of ethanol and neuropeptides

Ethanol neurotoxicity in culture: Selective loss of cholinergic neurons

“…phenotypic expression Vernadakis, 1990a, 1992;Rahman et al, 1994a) and survival (Kentroti and Vernadakis , 199 1 a;Rahman et al, 1994b), are affected by prenatal ethanol exposure. Previous reports from our laboratory have demonstrated that exposure of chick embryos to ethanol at an early stage of embryogenesis (days 1-3 of development), when neuroblasts remain pluripotential, results in decreased cholinergic and increased catecholaminergic and GABAergic expression in whole brain and cerebral hemispheres when examined at embryonic day 8 (Kentroti and Vernadakis, 1990a, 1991a, 1992. Furthermore, we have found that ethanol administration in ovo during this critical period decreases overall survival of neuroblasts in culture (Kentroti and Vernadakis, 1991b).…”

Correlation between morphological and biochemical effects of ethanol on neuroblast‐enriched cultures derived from three‐day‐old chick embryos

“…Alternatively, ethanol may interfere with the uptake or binding of substances from the nutrient medium and serum that are important for neurite growth, elongation, and migration. This theory is supported by studies from our laboratory in which cotreatment of embryos with NGF, EGF, or the neurotrophic peptides, GHRH or SRIF, attenuated the cholinotoxic effects of ethanol (Brodie et al, 1990;Kentroti and Vernadakis, 1990). Low concentrations of glutamate have also been demonstrated to stimulate neurite outgrowth and elongation (Pearce et al, 1987;Bulloch, 1989).…”

“…Choline acetyltransferase (ChAT) activity was measured by the radiometric method of Fonnum (1975) as modified in our laboratory for cell culture Kentroti and Vernadakis, 1990). This method employs a reaction catalyzed by tissue ChAT in which [3H]acetyl-CoA and unlabelled choline react to yield [3H]acetylcholine.…”

“…We have reported that ethanol markedly decreases cholinergic neuronal expression and enhances catecholaminergic neuronal expression as assessed by choline acetyltransferase (ChAT) and tyrosine hydrox ylase (TH) activities, respectively, when administered to chick embryos in ovo at early embryogenesis (Brodie and Vernadakis, 1990;Kentroti and Vernadakis, 1990). In order to delineate the effects of ethanol at a more direct cellular level, we have initiated studies using neural culture, a valuable experimental tool for studying growth phenomena, regulatory factors for growth and pharmacological manipulations (Vernadakis and Culver, 1980;Kapoor et al, 1988).…”

Differential expression in glial cells derived from chick embryo cerebral hemispheres at an advanced stage of development

“…This study focuses on the marked differences between those glia (E3) and glial populations from more advanced stages of development (E15) with respect to differentiation and phenotypic expression. In a series of related studies, we have shown that prenatal ethanol exposure markedly alters both morphological and biochemical properties of developing neurons both in ovo and in culture (Kentroti and Vernadakis, 1990;Rahman et al, 1993Rahman et al, , 1994a and, more importantly, that the effects are restricted to a critical period of sensitivity occurring very early during development (Kentroti and Vernadakis, 1990). These data attest to the profound differences in the same cell populations (both neurons and glia) when examined at different stages of development.…”