Schizophrenia, sensory gating, and nicotinic receptors
Schizophrenia, sensory gating, and nicotinic receptors
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DOI：
10.1093/oxfordjournals.schbul.a033320
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发表时间：
1998-01-01
影响因子：
6.6
通讯作者：
Freedman, R
中科院分区：
文献类型：
--
作者：
Adler, LE;Olincy, A;Freedman, R
一系列人类和动物研究表明，α 7-烟碱胆碱能受体的表达和功能改变可能是精神分裂症患者及其亲属听觉感觉门控缺陷的原因，其特征在于对重复刺激的听觉诱发反应（P50）的抑制减弱。这一发现，结合证据的家族传播的这种感觉门控缺陷，表明致病作用的α 7-烟碱受体的基因在精神分裂症。本文认为，这种功能障碍的可能影响在更广泛的背景下。这种功能障碍不仅与感觉门控困难一致，而且还可能使患者容易出现学习效率和准确性问题。这种学习问题可能是精神分裂症患者妄想、幻觉和社会功能障碍的基础。此外，许多精神分裂症患者的大量吸烟与激活受体所需的高浓度尼古丁以及受体的极快速脱敏是一致的。最后，该受体在细胞中的可能作用。生长和分化应与精神分裂症的发育缺陷和其他细胞异常联系起来考虑。
A series of human and animal investigations has suggested that altered expression and function of the alpha 7-nicotinic cholinergic receptor may be responsible for the auditory sensory gating deficit characterized in schizophrenia patients and their relatives as diminished suppression of an auditory-evoked response (P50) to repeated stimuli. This finding, in conjunction with evidence for familial transmission of this sensory gating deficit; suggests a pathogenic role of the gene for the alpha 7-nicotinic receptor in schizophrenia. This article considers the possible effects of this dysfunction in a broader context. Not only is this dysfunction consistent with difficulties in sensory gating, but it might also predispose patients to problems with learning efficiency and accuracy. Such learning problems could underlie schizophrenia patients' delusional thinking, hallucinations, and social dysfunction, In addition, heavy smoking in many schizophrenia patients is consistent with the high concentration of nicotine necessary to activate the receptor and with the receptor's extremely rapid desensitization. Finally, the receptor's possible role in cell. growth and differentiation should be considered in connection with developmental deficits and other cellular abnormalities in schizophrenia.