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- W2015761233 abstract "Ethanol may produce its toxicity during early neurogenesis by: 1. affecting the survival of neurons 2. preventing neuronal attachment to substrates of growth 3. inhibiting neuronal process formation 4. preventing neuronal interaction with neurotrophic materials or by 5. inhibiting neuronal production of neurotrophic materials. We have previously described that ethanol produces dose-dependent inhibition of neurite outgrowth (Pediatr Res 18:1248, 1984). In the present studies ethanol was shown to inhiblt process formation on a variety of biological substrates with no effect on neuronal survival or substrate attachment at the 50 % toxic dose (TD50) of ethanol for process formation. The binding of Nerve Growth Factor to its receptor on sensory neurons was not inhibited by ethanol at the TD50. Ethanol did inhibit the production of autocrine neurotrophic material. The calcium channel antagonist diltiazem protected the neuron against the toxic effects of ethanol on process formation. These data suggest that the interaction of neuronal surface receptors with ligands within the extracellular environment are not influenced by ethanol, but that this xenobiotic affects neuronal metabolism by a mechanism involving the biological handling of calcium." @default.
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- W2015761233 date "1985-04-01" @default.
- W2015761233 modified "2023-09-26" @default.
- W2015761233 title "1281 EFFECTS OF ETHANOL ON NEURONAL PROCESS FORMATION AND NEUROTROPHIC FACTOR PRODUCTION IN VITRO" @default.
- W2015761233 doi "https://doi.org/10.1203/00006450-198504000-01305" @default.
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