Griffith J M, Waldo M, Adler L E, Freedman R
Dept. of Psychiatry, University of Colorado Health Sciences Center, Denver 80262.
Psychiatry Res. 1993 Oct;49(1):29-39. doi: 10.1016/0165-1781(93)90028-f.
Diminished suppression of the P50 component of the evoked potential following repeated auditory stimuli is one example of a deficit in elementary sensory processing in schizophrenia. Normal subjects suppress the P50 evoked potential to the second of two paired auditory stimuli. Although normal P50 suppression is occasionally observed in schizophrenic patients, it generally disappears with subsequent testing. The object of this experiment was to determine conditions for the reproducible normalization of P50 suppression in schizophrenic patients. After baseline recordings, 12 schizophrenic subjects were allowed to sleep for 10 minutes. The depth of sleep obtained was assessed by electroencephalography (EEG). Normalization of P50 suppression was observed for approximately 3 minutes in all subjects who entered slow wave sleep, but not in those whose EEG records remained desynchronized. Some change was even observed in subjects who had only persistent alpha waves. The amount of normalization was correlated with the deepest stage of sleep reached. Normal control subjects did not show this phenomenon but instead had a transient decrease in sensory gating after waking from sleep. The results suggest that schizophrenic patients may have a defect that causes a neuronal mechanism critical to sensory gating to fail after brief use, although its activity can be transiently restored by a short period of inactivity. A rapidly desensitized neurotransmitter receptor is one possible mechanism of such an effect.
重复听觉刺激后诱发电位的P50成分抑制减弱是精神分裂症基本感觉处理缺陷的一个例子。正常受试者会抑制对两个配对听觉刺激中第二个刺激的P50诱发电位。虽然在精神分裂症患者中偶尔会观察到正常的P50抑制,但在随后的测试中它通常会消失。本实验的目的是确定精神分裂症患者P50抑制可重复正常化的条件。在进行基线记录后,让12名精神分裂症受试者睡眠10分钟。通过脑电图(EEG)评估获得的睡眠深度。所有进入慢波睡眠的受试者中,P50抑制在大约3分钟内恢复正常,但脑电图记录仍保持去同步化的受试者则没有。甚至在仅有持续阿尔法波的受试者中也观察到了一些变化。正常化的程度与达到的最深睡眠阶段相关。正常对照受试者没有表现出这种现象,而是在从睡眠中醒来后感觉门控有短暂下降。结果表明,精神分裂症患者可能存在一种缺陷,导致对感觉门控至关重要的神经元机制在短暂使用后失效,尽管其活动可通过短时间的不活动而暂时恢复。快速脱敏的神经递质受体是这种效应的一种可能机制。