Griffith J M, Freedman R
Department of Psychiatry, University of Texas, Dallas 75216, USA.
Psychiatry Res. 1995 Apr 28;56(3):271-8. doi: 10.1016/0165-1781(95)02516-y.
Diminished suppression of the P50 response to repeated auditory stimuli is one example of a deficit in elementary sensory processing in schizophrenia. Normal subjects suppress the response to the second of two paired auditory stimuli. Although normal suppression is occasionally observed in schizophrenic patients, it generally disappears with subsequent testing. We have previously reported that slow wave sleep (SWS) transiently normalized suppression in schizophrenic patients and that the degree of suppression was positively correlated with the depth of SWS attained. We hypothesized that schizophrenic patients may have a defect that causes a neuronal mechanism to fail after brief use and that its activity can be restored by a transient period of inactivity. The present study examined whether this effect of sleep in schizophrenic patients is specific to SWS or is due to nonspecific factors involved in any period of unconsciousness. After baseline recordings, 10 schizophrenic subjects were allowed a period of sleep until they attained rapid-eye-movement (REM) sleep. They were awakened at the end of the REM period, and postsleep recordings were obtained. REM-stage sleep failed to normalize suppression in any of the schizophrenic subjects. P50 suppression was subsequently assessed after a period of non-REM (NREM) sleep. Subjects who reached stage-2 sleep did demonstrate a transient correction in auditory gating. These results replicate our previous findings and suggest that the sleep effect is specific to NREM sleep. A desensitized nicotinic receptor that is resensitized during cholinergic inactivity in NREM sleep is one possible mechanism for this effect.
对重复听觉刺激的P50反应抑制减弱是精神分裂症基本感觉加工缺陷的一个例子。正常受试者会抑制对两个配对听觉刺激中第二个刺激的反应。虽然精神分裂症患者偶尔也会出现正常的抑制现象，但在后续测试中这种现象通常会消失。我们之前曾报道，慢波睡眠（SWS）可使精神分裂症患者的抑制现象暂时恢复正常，且抑制程度与达到的SWS深度呈正相关。我们推测，精神分裂症患者可能存在一种缺陷，导致神经元机制在短暂使用后失效，而其活动可通过一段短暂的不活动期得以恢复。本研究探讨了精神分裂症患者睡眠的这种效应是特定于SWS，还是由任何无意识时期涉及的非特异性因素所致。在进行基线记录后，10名精神分裂症受试者被允许睡眠一段时间，直到进入快速眼动（REM）睡眠。在REM期结束时将他们唤醒，并进行睡眠后记录。REM期睡眠未能使任何精神分裂症受试者的抑制现象恢复正常。随后在一段非快速眼动（NREM）睡眠后评估P50抑制情况。进入2期睡眠的受试者确实表现出听觉门控的短暂纠正。这些结果重复了我们之前的发现，并表明睡眠效应特定于NREM睡眠。一种在NREM睡眠胆碱能不活动期间重新敏感化的脱敏烟碱受体是产生这种效应的一种可能机制。
