Nicotinic modulation of human auditory sensory memory: Evidence from mismatch negativity potentials
Nicotinic modulation of human auditory sensory memory: Evidence from mismatch negativity potentials
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DOI：
10.1016/j.ijpsycho.2005.07.014
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发表时间：
2006-01-01
影响因子：
3
通讯作者：
Stephan, KE
中科院分区：
文献类型：
--
作者：
Baldeweg, T;Wong, D;Stephan, KE
错配负波（MMN）产生的损害是精神分裂症的一个可靠的生物学标志。了解其产生所涉及的生理和药理学过程，因此可能会推进我们对这种复杂的disorder.The本研究测试，如果急性管理尼古丁调节人类听觉感觉记忆与MMN测量。使用连续变化（巡回）标准刺激的刺激方案记录对音调持续时间偏差的ERP反应，以测量刺激重复对新刺激编码的影响（MMN记忆痕迹效应）。20名健康成年志愿者被随机分配接受尼古丁口香糖或安慰剂治疗，与基线记录相比，尼古丁治疗组的MMN振幅增加。而安慰剂组MMN无变化。药物作用是由于选择性增强额叶正电位的标准刺激（从80-200毫秒刺激后），而负偏差保持不受影响。此外，在尼古丁刺激下，这种重复积极性表现出更显着的增加与刺激重复相比，基线和placebo.These结果有潜在的意义，精神分裂症的尼古丁激动剂可以改善患者的MMN缺陷，通过改善刺激编码和感觉记忆痕迹的形成。(c)2005 Elsevier B. V.保留所有权利。
Impairment in mismatch negativity (MMN) generation is a robust biological marker of schizophrenia. Understanding the physiological and pharmacological processes involved in its generation may therefore advance our understanding of this complex disorder.The present study tested if acute administration of nicotine modulates human auditory sensory memory as measured with MMN. ERP responses to tone duration deviants were recorded using a stimulation protocol with Continuously changing (roving) standard stimuli in order to measure the effect of stimulus repetitions on encoding of new stimuli (MMN memory trace effect). Twenty healthy adult Volunteers were randomly assigned to receive either a nicotine gum or placebo after a baseline ERP recording.Nicotine administration augmented MMN amplitude in the treatment group compared to the baseline recording. while no MMN change was found in the placebo group. The drug effect was due to a selective enhancement of a frontal positive potential to standard stimuli (from 80-200 ms post-stimulus), while the negativity to deviants remained unaffected. Furthermore, under nicotine Stimulation this repetition positivity showed a more marked increase with stimulus repetition compared to baseline and placebo.These results have potential implications for schizophrenia by suggesting that nicotinic agonists could ameliorate patients' MMN deficits by improving stimulus encoding and sensory memory trace formation. (c) 2005 Elsevier B.V. All rights reserved.