4.6 Article

Inhibition of Cortical Activity and Apoptosis Caused by Ethanol in Neonatal Rats In Vivo

期刊

CEREBRAL CORTEX
卷 27, 期 2, 页码 1068-1082

出版社

OXFORD UNIV PRESS INC
DOI: 10.1093/cercor/bhv293

关键词

apoptosis; electroencephalogram; ethanol; fetal alcohol syndrome; neonate; neuronal network; rat; sensory-evoked potentials

资金

  1. Fondation pour la Recherche Medicale [DEQ20110421301]
  2. Government of the Russian Federation [11.G34.31.0075]
  3. Ministry of Education and Research
  4. Kazan Federal University

向作者/读者索取更多资源

Alcohol consumption during pregnancy causes fetal alcohol spectrum disorder, which includes neuroapoptosis and neurobehavioral deficits. The neuroapoptotic effects of alcohol have been hypothesized to involve suppression of brain activity. However, in vitro studies suggest that ethanol acts as a potent stimulant of cortical activity. We explored the effects of alcohol (1-6 g/kg) on electrical activity in the rat somatosensory cortex in vivo at postnatal days P1-23 and compared them with its apoptotic actions. At P4-7, when the peak of alcohol-induced apoptosis was observed, alcohol strongly suppressed spontaneous gamma and spindle-bursts and almost completely silenced neurons in a dose-dependent manner. The dose-dependence of suppression of neuronal activity strongly correlated with the alcohol-induced neuroapoptosis. Alcohol also profoundly inhibited sensory-evoked bursts and suppressed motor activity, a physiological trigger of cortical activity bursts in newborns. The suppressive effects of ethanol on neuronal activity waned during the second and third postnatal weeks, when instead of silencing the cortex, alcohol evoked delta-wave electrographic activity. Thus, the effects of alcohol on brain activity are strongly age-dependent, and during the first postnatal week alcohol profoundly inhibits brain activity. Our findings suggest that the adverse effects of alcohol in the developing brain involve suppression of neuronal activity.

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