Abduljawad K A, Langley R W, Bradshaw C M, Szabadi E
Division of Psychiatry, University of Nottingham, UK.
J Psychopharmacol. 2001 Dec;15(4):237-42. doi: 10.1177/026988110101500402.
Contraction of the orbicularis oculi muscle in response to a sudden loud sound (acoustic startle response) and the N1/P2 component of the auditory evoked potential are both attenuated when a brief low-intensity stimulus is presented 30-500 ms before the 'startle-eliciting' stimulus (prepulse inhibition). We examined the effects of two sedative/anxiolytic drugs, diazepam and clonidine, on prepulse inhibition of these two responses in healthy volunteers. Fifteen males (aged 18-35 years) participated in three sessions in which they received oral doses of placebo, diazepam 10 mg and clonidine 0.2 mg according to a balanced double-blind protocol. Thirty-minute simultaneous recordings of the electromyographic (EMG) responses of the orbicularis oculi muscle of the right eye and the vertex auditory evoked potentials took place 120 min after ingestion of clonidine and 60 min after ingestion of diazepam. Sound stimuli (1 kHz) were presented in 60 trials separated by variable intervals (mean 25 s): (i) 40-ms 115-dB ('pulse alone', 20 trials); (ii) 40-ms 85-dB (20 trials); (iii) 40-ms 85-dB, followed after 120 ms by 40-ms 115-dB ('prepulse/pulse', 20 trials). Mean amplitudes of the EMG response and the N1/P2 potential were derived from the pulse-alone trials and, in each case, percentage prepulse inhibition was calculated. The amplitude of the EMG response was significantly reduced both by diazepam and by clonidine; neither drug significantly altered prepulse inhibition of the EMG response. Diazepam, but not clonidine, significantly reduced the amplitude of the N1/P2 potential; neither drug significantly affected prepulse inhibition of the N1/P2 potential. Both drugs reduced self-rated alertness and anxiety, and systolic blood pressure; clonidine, but not diazepam reduced diastolic blood pressure and salivation. The results confirm previous findings that sedative drugs can suppress the startle response without affecting prepulse inhibition of this response, and provide new information on the effects of these drugs on the N1/P2 potential and its inhibition by prepulses.
当在引发惊吓的刺激之前30 - 500毫秒呈现一个短暂的低强度刺激时（预脉冲抑制），眼轮匝肌对突然的大声响的收缩反应（听觉惊吓反应）以及听觉诱发电位的N1/P2成分都会减弱。我们研究了两种镇静/抗焦虑药物，地西泮和可乐定，对健康志愿者这两种反应的预脉冲抑制的影响。15名男性（年龄在18 - 35岁之间）参与了三个阶段的实验，按照平衡双盲方案，他们分别口服安慰剂、10毫克地西泮和0.2毫克可乐定。在摄入可乐定120分钟后以及摄入地西泮60分钟后，对右眼眼轮匝肌的肌电图（EMG）反应和头顶听觉诱发电位进行了30分钟的同步记录。声音刺激（1千赫）以60次试验呈现，试验间隔可变（平均25秒）：（i）40毫秒115分贝（“单独脉冲”，20次试验）；（ii）40毫秒85分贝（20次试验）；（iii）40毫秒85分贝，在120毫秒后接着40毫秒115分贝（“预脉冲/脉冲”，20次试验）。EMG反应和N1/P2电位的平均幅度来自单独脉冲试验，并且在每种情况下，计算预脉冲抑制百分比。地西泮和可乐定都显著降低了EMG反应的幅度；两种药物均未显著改变EMG反应的预脉冲抑制。地西泮而非可乐定显著降低了N1/P2电位的幅度；两种药物均未显著影响N1/P2电位的预脉冲抑制。两种药物都降低了自我评定的警觉性和焦虑以及收缩压；可乐定而非地西泮降低了舒张压和唾液分泌。结果证实了先前的发现，即镇静药物可以抑制惊吓反应而不影响该反应的预脉冲抑制，并提供了关于这些药物对N1/P2电位及其预脉冲抑制作用的新信息。
