Normalization of the auditory P50 gating deficit of schizophrenic patients after non-REM but not REM sleep.

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.