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精神分裂症患者与正常受试者的听觉感觉门控和儿茶酚胺代谢

Auditory sensory gating and catecholamine metabolism in schizophrenic and normal subjects.

作者信息

Waldo M, Gerhardt G, Baker N, Drebing C, Adler L, Freedman R

机构信息

Department of Psychiatry, Denver Veterans Administration Medical Center, CO.

出版信息

Psychiatry Res. 1992 Oct;44(1):21-32. doi: 10.1016/0165-1781(92)90066-c.

DOI:10.1016/0165-1781(92)90066-c
PMID:1461944
Abstract

Diminished neuronal response to repeated sensory input is a sensory-gating phenomenon that has been found to be deficient in schizophrenic patients. For example, schizophrenic patients fail to decrease the amplitude of the P50 wave of the auditory evoked potential to the second of paired click stimuli. In some studies, however, normal subjects have also failed to decrease their P50 responses. The aim of this study was to determine if accommodation to the recording situation over time would affect the gating of the P50 response. The gating of the P50 wave is measured as the ratio of the amplitude of the second response to the amplitude of the first. Three successive auditory evoked potentials were compiled, each from trains of 32 pairs of stimuli. Twelve normal subjects and 12 schizophrenic patients were studied. Unconjugated catecholamine metabolites were measured from venous samples drawn before and after the electrophysiological recording. Between the first and third trials, the normal subjects significantly increased their gating of P50. This increase in gating of P50 was related to decreased levels of the noradrenergic metabolite 3-methoxy-4-hydroxyphenylglycol. No similar phenomenon was observed in the schizophrenic patients, a number of whom had a further decrease in P50 gating over the three trials. Transient failure to observe gating of P50 in normal subjects may be related to increased state-dependent noradrenergic activity, which is known to disrupt sensory gating. This mechanism does not seem to account for the more persistent failure of sensory gating in schizophrenia.

摘要

神经元对重复感觉输入的反应减弱是一种感觉门控现象,已发现精神分裂症患者存在这种现象的缺陷。例如,精神分裂症患者在对成对点击刺激中的第二个刺激产生的听觉诱发电位的P50波幅上未能降低。然而,在一些研究中,正常受试者也未能降低他们的P50反应。本研究的目的是确定随着时间推移对记录情况的适应是否会影响P50反应的门控。P50波的门控以第二个反应的幅度与第一个反应的幅度之比来衡量。收集了连续三次听觉诱发电位,每次均来自32对刺激序列。研究了12名正常受试者和12名精神分裂症患者。在电生理记录前后采集静脉血样,测量未结合儿茶酚胺代谢产物。在第一次和第三次试验之间,正常受试者显著提高了他们对P50的门控。P50门控的这种增加与去甲肾上腺素能代谢产物3-甲氧基-4-羟基苯乙二醇水平的降低有关。在精神分裂症患者中未观察到类似现象,其中一些患者在三次试验中P50门控进一步降低。正常受试者中短暂未能观察到P50门控可能与状态依赖性去甲肾上腺素能活动增加有关,已知这种活动会破坏感觉门控。这种机制似乎无法解释精神分裂症中更持续的感觉门控失败。

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