Different dose levels of ethanol (2,3,4,5 g/kg) were administered to rat pups between postnatal days 4 and 10. Ethanol caused a dose-dependent decrease in brain weight (measured on postnatal day 12) and inhibition of carbachol-stimulated phosphoinositide metabolism (measured in cerebral cortex slices on postnatal day 7). The 2 g/kg dose, which gave blood alcohol levels of 128 mg/dl, was a no-effect-level for both endpoints. Ethanol administration did not alter the relative distribution of phosphoinositides in the cerebral cortex from 7 day-old rats. These results show a dose-dependent correlation between ethanol-induced microencephaly and inhibition of muscarinic receptor-stimulated phosphoinositide metabolism and add support to the hypothesis that this second messenger system may be involved in the developmental neurotoxicity of ethanol.

Administration of ethanol during brain growth spurt causes dose-dependent microencephaly and inhibition of muscarinic receptor-stimulated phosphoinositide metabolism in the rat / F. Reno', X.X. Tan, W. Balduini, L.G. Costa. - In: RESEARCH COMMUNICATIONS IN ALCOHOL AND SUBSTANCES ABUSE. - ISSN 1080-8388. - 15:3-4(1994), pp. 141-150.

Administration of ethanol during brain growth spurt causes dose-dependent microencephaly and inhibition of muscarinic receptor-stimulated phosphoinositide metabolism in the rat

F. Reno'
Primo
;
1994

Abstract

Different dose levels of ethanol (2,3,4,5 g/kg) were administered to rat pups between postnatal days 4 and 10. Ethanol caused a dose-dependent decrease in brain weight (measured on postnatal day 12) and inhibition of carbachol-stimulated phosphoinositide metabolism (measured in cerebral cortex slices on postnatal day 7). The 2 g/kg dose, which gave blood alcohol levels of 128 mg/dl, was a no-effect-level for both endpoints. Ethanol administration did not alter the relative distribution of phosphoinositides in the cerebral cortex from 7 day-old rats. These results show a dose-dependent correlation between ethanol-induced microencephaly and inhibition of muscarinic receptor-stimulated phosphoinositide metabolism and add support to the hypothesis that this second messenger system may be involved in the developmental neurotoxicity of ethanol.
Settore BIO/16 - Anatomia Umana
1994
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/1019829
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