NEUROBIOLOGICAL STUDIES OF SENSORY GATING IN SCHIZOPHRENIA
NEUROBIOLOGICAL STUDIES OF SENSORY GATING IN SCHIZOPHRENIA
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DOI：
10.1093/schbul/13.4.669
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发表时间：
1987-01-01
影响因子：
6.6
通讯作者：
FRANKS, R
中科院分区：
文献类型：
--
作者：
FREEDMAN, R;ADLER, LE;FRANKS, R
精神分裂症的感觉障碍通常被描述为无法从有意义的感觉输入中过滤掉外来噪音。这种无法过滤的神经生物学基础已经用听觉诱发电位进行了研究，听觉诱发电位是大脑对声音的电反应的计算机化平均值。这些声音成对出现是为了测试大脑抑制或控制对重复刺激的反应的能力。精神分裂症患者缺乏门控特定波（P50波）所显示的神经元反应的能力。在人类受试者中对这种缺陷的测量以及在动物中对其神经生物学的探索，为精神分裂症的病理生理学中的几个问题提供了证据：（1）多巴胺在用精神安定药物治疗的精神分裂症患者中感觉功能改善中的作用，（2）精神分裂症患者中感觉功能的家族或遗传缺陷与多巴胺代谢的可能异常之间的相互作用，以及（3）躁狂症和其他精神疾病中去甲肾上腺素能亢进可能模仿精神分裂症中某些病理生理缺陷的机制。
The sensory disturbance in schizophrenia is often described as an inability to filter out extraneous noise from meaningful sensory inputs. The neurobiological basis of this inability to filter has been examined using auditory evoked potentials, which are computerized averages of the brain's electrical response to sound. The sounds are presented in pairs to test the ability of the brain to inhibit, or gate, its response to a repeated stimulus. Schizophrenic patients lack the ability to gate the neuronal response shown by a particular wave, the P50wave. The measurement of this deficit in human subjects and the exploration of its neurobiology in animals has produced evidence about several issues in the pathophysiology of schizophrenia: (1) the role of dopamine in improvement of sensory function in schizophrenic patients treated with neuroleptic drugs, (2) the interaction between familial or genetic deficits in sensory functioning in schizophrenic patients and possible abnormalities in dopamine metabolism, and (3) a mechanism by which noradrenergic hyperactivity in mania and other psychiatric illnesses might mimic some pathophysiological deficits in schizophrenia.