PDF(Pubmed)
Abstract：
BACKGROUND: Impairment in auditory sensory gating (ASG) has been documented in alcohol dependence [1]. Likewise, it has been shown that ASG becomes abnormal during alcohol administration in otherwise healthy individuals [2]. Patterns of gating abnormality associated with alcohol use are likely associated with an alcohol responsive neurochemical like glutamate (Glu), particularly since it is well-established that alcohol affects NMDA receptors and that glutamatergic functioning is abnormal in both acute alcohol use and in alcohol dependence [3]. Hence, a link between Glu metabolite levels and ASG was hypothesized. It was first hypothesized that Glu and ASG abnormality would be found in groups with alcohol dependence. A second hypothesis was that across groups, greater Glu would predict reduced ASG.
METHODS: Groups were comprised of healthy, non-drinking controls (Controls, N = 4), individuals with current alcohol dependence (AUD-current, N = 6), and with alcohol dependence in remission for at least 1 year (AUD-remission, N = 6). Participants underwent a diagnostic assessment for alcohol consumption, MRI, 1H-MRS for in vivo assessment of Glu and other metabolites, and MEG scanning during a paired click protocol. ASG was computed as the ratio of the source strength of the 50 ms component in the event related field (ERF) to the second click in the pair divided by the source strength of the 50 ms component to the first click in the pair.
RESULTS: Univariate MANOVAs controlling for age and gender revealed a significant effect for group on Glu and ASG, such that ASG ratios were significantly elevated, implying weakened gating. Glu concentration was reduced in AUD-current relative to the other two groups. Further analysis revealed that when additionally controlling for the group effect, reduced Glu predicted increasing impairment in ASG.
CONCLUSIONS: The overall results were consistent with the hypothesis that differences in Glu metabolite levels associated with alcohol dependence result in impaired ASG.
METHODS: Groups were comprised of healthy, non-drinking controls (Controls, N = 4), individuals with current alcohol dependence (AUD-current, N = 6), and with alcohol dependence in remission for at least 1 year (AUD-remission, N = 6). Participants underwent a diagnostic assessment for alcohol consumption, MRI, 1H-MRS for in vivo assessment of Glu and other metabolites, and MEG scanning during a paired click protocol. ASG was computed as the ratio of the source strength of the 50 ms component in the event related field (ERF) to the second click in the pair divided by the source strength of the 50 ms component to the first click in the pair.
RESULTS: Univariate MANOVAs controlling for age and gender revealed a significant effect for group on Glu and ASG, such that ASG ratios were significantly elevated, implying weakened gating. Glu concentration was reduced in AUD-current relative to the other two groups. Further analysis revealed that when additionally controlling for the group effect, reduced Glu predicted increasing impairment in ASG.
CONCLUSIONS: The overall results were consistent with the hypothesis that differences in Glu metabolite levels associated with alcohol dependence result in impaired ASG.
摘要：
背景：听觉感觉门控（ASG）受损已在酒精依赖中得到证实[1]。同样，研究表明，在其他方面健康的个体中，在酒精给药期间，ASG变得异常[2]。与酒精使用相关的门控异常模式可能与酒精反应性神经化学物质如谷氨酸（Glu）相关，特别是由于已确定酒精会影响NMDA受体，并且在急性酒精使用和酒精依赖中，谷氨酸能功能异常[3]。因此，假设Glu代谢物水平与ASG之间存在联系.首先假设在酒精依赖组中发现Glu和ASG异常。第二个假设是跨群体，更高的Glu会预测ASG降低。
方法：组由健康、非饮酒控制(控制，N=4),目前有酒精依赖的个体(AUD-current，N=6),并且酒精依赖缓解至少1年(AUD-缓解，N=6)。参与者接受了酒精消费的诊断评估，MRI,1H-MRS用于体内评估Glu和其他代谢物，和MEG扫描在配对的点击协议。ASG被计算为事件相关字段(ERF)中的50ms分量的源强度与该对中的第二次点击的比率除以50ms分量与该对中的第一次点击的源强度。
结果：控制年龄和性别的单变量MANOVAs显示对Glu和ASG有显著影响，因此ASG比率显著升高，暗示弱化的门控。相对于其他两组,AUD-电流中的Glu浓度降低。进一步的分析表明，当额外控制群体效应时，Glu降低预测ASG损伤增加。
结论：总体结果与与酒精依赖相关的Glu代谢物水平差异导致ASG受损的假设一致。
方法：组由健康、非饮酒控制(控制，N=4),目前有酒精依赖的个体(AUD-current，N=6),并且酒精依赖缓解至少1年(AUD-缓解，N=6)。参与者接受了酒精消费的诊断评估，MRI,1H-MRS用于体内评估Glu和其他代谢物，和MEG扫描在配对的点击协议。ASG被计算为事件相关字段(ERF)中的50ms分量的源强度与该对中的第二次点击的比率除以50ms分量与该对中的第一次点击的源强度。
结果：控制年龄和性别的单变量MANOVAs显示对Glu和ASG有显著影响，因此ASG比率显著升高，暗示弱化的门控。相对于其他两组,AUD-电流中的Glu浓度降低。进一步的分析表明，当额外控制群体效应时，Glu降低预测ASG损伤增加。
结论：总体结果与与酒精依赖相关的Glu代谢物水平差异导致ASG受损的假设一致。
