Knott V J
Adult Outpatient Department, Royal Ottawa Hospital, Ontario, Canada.
Addict Behav. 1987;12(4):375-9. doi: 10.1016/0306-4603(87)90053-0.
Reports of tobacco-induced electrocortical activation have frequently indicated that this effect is mediated via nicotine's action on sub-cortical structures. This study focused on human brain stem involvement by examining the acute effects of tobacco smoking on brain stem auditory potentials (BSAEPs). Twelve regular smokers were tested on two separate sessions involving sham or real smoking. On each session, BSAEPs were recorded during a baseline period and immediately after smoking. BSAEPs, recorded from Cz, were elicited by presentation of 1,000 monaural, rare fraction click stimuli. Latency and amplitudes of peak components I, III and V were assessed and analysed. No significant effects were observed for latency measures or for amplitudes of peaks I and III. A significant effect was observed for peak V with tobacco resulting in larger amplitudes relative to sham smoking. Peak V reflects activity from upper pontine-lower midbrain sites and this tobacco-peak V finding is discussed in relation to arousal and information processing theories of smoking.
关于烟草诱导的皮质电激活的报告经常表明,这种效应是通过尼古丁对皮质下结构的作用介导的。本研究通过检查吸烟对脑干听觉诱发电位(BSAEP)的急性影响,聚焦于人类脑干的参与情况。12名经常吸烟者在两个不同的环节接受测试,分别涉及假吸烟或真吸烟。在每个环节中,在基线期和吸烟后立即记录BSAEP。从Cz记录的BSAEP由呈现1000个单耳、稀疏率点击刺激诱发。评估并分析了峰成分I、III和V的潜伏期和振幅。潜伏期测量以及峰I和峰III的振幅均未观察到显著影响。观察到峰V有显著影响,吸烟相对于假吸烟导致更大的振幅。峰V反映了脑桥上段-中脑下段部位的活动,并且结合吸烟的唤醒和信息处理理论对这一烟草-峰V的发现进行了讨论。