Slawecki Craig J
Scripps Research Institute, Department of Neuropharmacology, La Jolla, California 92037, USA.
Alcohol Clin Exp Res. 2002 Feb;26(2):246-54.
Adolescent ethanol (EtOH) exposure is a significant health concern due to the potential long-term effects of EtOH on the developing brain. However, few studies have assessed how exposure to EtOH during adolescence influences the response of adults to EtOH after a long period of withdrawal. This study was designed to assess long-term changes in EEG activity after EtOH challenge in adult rats exposed to EtOH during adolescence.
Male Sprague Dawley rats (n = 24) were exposed to EtOH vapor for 5 days (12 hr/day) between postnatal days 35 and 40. After maturing to adulthood, rats were implanted with cortical, amygdalar, and hippocampal electrodes. Then EEG activity after EtOH challenge (0.0-1.5 g/kg) was assessed.
There were no EEG differences between groups under baseline or vehicle conditions, but EtOH did have differential behavioral and electrophysiological effects when adolescent ethanol-exposed rats were compared with controls. After 1.5 g/kg EtOH, ethanol-exposed rats displayed decreased behavioral indexes of intoxication. In addition, EtOH significantly increased 4 to 6 Hz power in the hippocampus and parietal cortex of the control group but had no effect on 4 to 6 Hz power in the ethanol-exposed group in either of these brain regions. EtOH produced maximal increases in cortical EEG variability in control rats after 1.5 g/kg EtOH but produced maximal increases in cortical EEG variability in ethanol-exposed rats after 1.0 g/kg EtOH. As a result, ethanol-induced increases in EEG variability after 1.5 g/kg ethanol were blunted in the ethanol-exposed group compared with the control group.
These data demonstrate persistent and brain-region-specific changes in the neurobehavioral effects of acute EtOH challenge in adult rats exposed to EtOH during adolescence in the absence of baseline neurophysiological differences. Decreased EEG responses to high doses of EtOH combined with decreased behavioral measures of intoxication suggest that adolescent ethanol exposure produces long-lasting tolerance to the sedative effects of ethanol.
青少年乙醇（EtOH）暴露是一个重大的健康问题，因为EtOH对发育中的大脑可能产生长期影响。然而，很少有研究评估青少年时期暴露于EtOH如何影响成年人在长期戒断后对EtOH的反应。本研究旨在评估青春期暴露于EtOH的成年大鼠在接受EtOH刺激后脑电图（EEG）活动的长期变化。
雄性Sprague Dawley大鼠（n = 24）在出生后第35天至40天期间暴露于EtOH蒸气中5天（每天12小时）。成年后，给大鼠植入皮质、杏仁核和海马电极。然后评估EtOH刺激（0.0 - 1.5 g/kg）后的EEG活动。
在基线或给予赋形剂条件下，两组之间的EEG没有差异，但与对照组相比，青春期暴露于乙醇的大鼠在接受EtOH刺激时确实有不同的行为和电生理效应。给予1.5 g/kg EtOH后，暴露于乙醇的大鼠中毒行为指标降低。此外，EtOH显著增加了对照组海马和顶叶皮质中4至6 Hz的功率，但在这两个脑区中，对暴露于乙醇的大鼠的4至6 Hz功率没有影响。给予1.5 g/kg EtOH后，EtOH使对照组大鼠皮质EEG变异性最大增加，但给予1.0 g/kg EtOH后，使暴露于乙醇的大鼠皮质EEG变异性最大增加。结果，与对照组相比，暴露于乙醇的组在给予1.5 g/kg乙醇后，乙醇诱导的EEG变异性增加减弱。
这些数据表明，在没有基线神经生理差异的情况下，青春期暴露于EtOH的成年大鼠在接受急性EtOH刺激时，神经行为效应存在持续且脑区特异性的变化。对高剂量EtOH的EEG反应降低，同时中毒行为指标降低，表明青春期乙醇暴露会对乙醇的镇静作用产生持久的耐受性。
