Slawecki C J, Betancourt M, Li T K, Ehlers C L
The Scripps Research Institute, Department of Neuropharmacoloy, La Jolla, California 92037, USA.
Alcohol Clin Exp Res. 2000 Oct;24(10):1492-9.
Specific neurophysiological profiles, such as reduced P300 amplitude or altered spectral power in the EEG, have been associated with a risk for alcoholism in several clinical populations. In certain rodent models, high versus low alcohol consumption is associated with similar neurophysiological differences. For example, alcohol-preferring (P) rats have increased spectral power and decreased P300 amplitudes compared with alcohol-nonpreferring (NP) rats. In the present study, the neurophysiological profiles of high-alcohol-drinking (HAD) and low-alcohol-drinking (LAD) rats were assessed (1) to determine if their electrophysiological profiles are similar to P and NP rats and (2) to examine the relationship of these neurophysiological indices to ethanol drinking.
Ethanol-naive HAD and LAD rats were implanted with cortical and amygdalar recording electrodes. Baseline EEG and event-related potentials (ERPs) then were assessed. Subsequently, all rats were trained to self-administer ethanol by using a sucrose-substitution procedure.
Baseline EEG and ERP (i.e., pre-ethanol exposure) were assessed based on line (HAD versus LAD) and actual ethanol consumption (high drinkers versus low drinkers). At baseline, ethanol-naive HAD rats displayed significantly greater power in the cortical EEG and decreased amygdala N1 ERP amplitude compared with ethanol-naive LAD rats. Similar EEG and ERP profiles have been observed when P and NP rats are compared. No differences in P300 between lines were observed, but high-drinking rats, independent of line, had significantly decreased P300 amplitude in the amygdala compared with low-drinking rats.
These data suggest there are some similarities in EEG and ERP profiles of P and HAD rats compared with NP and LAD rats. Furthermore, the data suggest that decreased P300 amplitude in the amygdala is associated with increased limited access ethanol drinking.
特定的神经生理特征,如脑电图中P300波幅降低或频谱功率改变,在多个临床群体中与酒精成瘾风险相关。在某些啮齿动物模型中,高酒精摄入量与低酒精摄入量也存在类似的神经生理差异。例如,与非嗜酒(NP)大鼠相比,嗜酒(P)大鼠的频谱功率增加,P300波幅降低。在本研究中,对高酒精摄入(HAD)和低酒精摄入(LAD)大鼠的神经生理特征进行评估,以确定它们的电生理特征是否与P和NP大鼠相似,并检验这些神经生理指标与乙醇摄入之间的关系。
对未接触过乙醇的HAD和LAD大鼠植入皮质和杏仁核记录电极,然后评估基线脑电图和事件相关电位(ERP)。随后,所有大鼠通过蔗糖替代程序接受自我给予乙醇的训练。
根据品系(HAD与LAD)和实际乙醇摄入量(高饮酒者与低饮酒者)评估基线脑电图和ERP(即乙醇暴露前)。在基线时,与未接触过乙醇的LAD大鼠相比,未接触过乙醇的HAD大鼠的皮质脑电图功率显著更高,杏仁核N1 ERP波幅降低。比较P和NP大鼠时也观察到类似的脑电图和ERP特征。品系之间未观察到P300的差异,但与低饮酒大鼠相比,高饮酒大鼠(无论品系)杏仁核中的P300波幅显著降低。
这些数据表明,与NP和LAD大鼠相比,P和HAD大鼠的脑电图和ERP特征存在一些相似之处。此外,数据表明杏仁核中P300波幅降低与有限接触乙醇的摄入量增加有关。