Gottesmann Claude
Département des Sciences de la Vie, Faculté des Sciences, Université de Nice-Sophia Antipolis, 06108 Nice Cedex 2, France.
Med Sci (Paris). 2006 Feb;22(2):201-5. doi: 10.1051/medsci/2006222201.
Normal waking mentation is the outcome of the combined action of both electrophysiological and neurochemical antagonistic and complementary activating and inhibitory influences occurring mainly in the cerebral cortex. The chemical ones are supported principally by acetylcholine, and noradrenaline and serotonin, respectively. During rapid eye movement (REM) sleep, the monoaminergic silence - except dopaminergic ongoing activity - disrupts this equilibrium and seems to be responsible for disturbances of mental activity characteristic of dreaming. This imbalance could cause disconnectivity of cortical areas, failure of latent inhibition and possibly the concomitant prefrontal dorsolateral deactivation. Moreover, the decrease of prefrontal dopaminergic functioning could explain the loss of reflectiveness in this sleep stage. All these phenomena are also encountered in schizophrenia. The psychotic-like mentation of dreaming (hallucinations, delusions, bizarre thought processes) could result from the disinhibition of dopamine influence in the nucleus accumbens by the noradrenergic and serotonergic local silence and/or the lifting of glutamate influence from the prefrontal cortex and hippocampus. We hypothesize that, during REM sleep, the increase of dopamine and the decrease of glutamate release observed in nucleus accumbens reach the threshold values at which psychotic disturbances arise during wakefulness. Whatever the precise mechanism, it seems that the functional state of the prefrontal cortex and nucleus accumbens is the same during dreaming sleep stage and in schizophrenia. The convergent psychological, electrophysiological, tomographic, pharmacological and neurochemical criteria of REM sleep and schizophrenia suggest that this sleep stage could become a good neurobiological model of this psychiatric disease.
正常清醒时的心理活动是主要发生在大脑皮层的电生理和神经化学的拮抗与互补的激活及抑制作用共同作用的结果。化学作用主要分别由乙酰胆碱、去甲肾上腺素和5-羟色胺支持。在快速眼动（REM）睡眠期间，单胺能沉默（多巴胺能持续活动除外）破坏了这种平衡，似乎是导致梦的特征性心理活动紊乱的原因。这种失衡可能导致皮层区域的失联、潜在抑制的失败以及可能伴随的前额叶背外侧失活。此外，前额叶多巴胺能功能的下降可以解释这个睡眠阶段反思能力的丧失。所有这些现象在精神分裂症中也会出现。梦的类精神病性心理活动（幻觉、妄想怪异的思维过程）可能是由于伏隔核中多巴胺影响的去抑制，通过去甲肾上腺素能和5-羟色胺能局部沉默和/或前额叶皮层和海马体谷氨酸影响的解除。我们假设，在快速眼动睡眠期间，伏隔核中观察到的多巴胺增加和谷氨酸释放减少达到了清醒时出现精神障碍的阈值。无论确切机制如何，似乎在梦的睡眠阶段和精神分裂症中，前额叶皮层和伏隔核的功能状态是相同的。快速眼动睡眠和精神分裂症在心理、电生理、断层扫描、药理学和神经化学标准上的趋同表明，这个睡眠阶段可能成为这种精神疾病的一个良好神经生物学模型。
