Pharmacology & Anaesthesiology Unit, School of Medicine and Pharmacology, The University of Western Australia, Centre for Clinical Research in Neuropsychiatry, Graylands Hospital, Australia.
Eur Neuropsychopharmacol. 2012 Oct;22(10):734-46. doi: 10.1016/j.euroneuro.2012.02.009. Epub 2012 Mar 21.
Auditory P3 amplitude reduction is one of the most robust and replicated findings in schizophrenia. Recent evidence suggests that these reductions are due to reductions in both power and phase-locking at delta and theta frequencies. We have previously shown that the auditory, but not visual, P3 is reduced in healthy participants given the catecholamine releasing agent dexamphetamine. Our aim was to determine whether the auditory P3 amplitude reduction induced by dexamphetamine has similar power and phase locking characteristics to that seen in schizophrenia. Forty-four healthy participants were given 0.45 mg/kg dexamphetamine and placebo, in a double-blinded, placebo-controlled, cross-over design. The task was a three-stimulus auditory odd-ball task, target stimuli were the major stimuli of interest. Individual target trials underwent wavelet analysis to give power and phase-locking of delta (3 Hz), theta (4-7 Hz), alpha (8-12 Hz), beta (13-30 Hz) and gamma (30-50 Hz) frequencies for a 50 ms time window centred around the peak of the target P3. Delta power around the P3 peak was significantly reduced when participants were given dexamphetamine. Delta phase-locking was also reduced but only when analysis was targeted at the location of the peak P3 amplitude. In contrast, theta power and phase-locking were not affected by dexamphetamine. These findings suggest that increased catecholamine activity may be responsible for the power and phase-locking reductions of the auditory P3 delta component in patients with schizophrenia. Interestingly, dexamphetamine significantly increased gamma power around the P3 peak. We attempt to link this finding with the gamma alterations that have been found in patients with schizophrenia.
听觉 P3 振幅降低是精神分裂症中最具稳健性和可重复性的发现之一。最近的证据表明,这些降低是由于 delta 和 theta 频率的功率和相位锁定的降低。我们之前已经表明,在给予儿茶酚胺释放剂苯丙胺的健康参与者中,听觉 P3 而不是视觉 P3 减少。我们的目的是确定苯丙胺诱导的听觉 P3 振幅降低是否具有与精神分裂症中所见相似的功率和相位锁定特征。44 名健康参与者接受了 0.45 mg/kg 苯丙胺和安慰剂,采用双盲、安慰剂对照、交叉设计。任务是三刺激听觉Oddball 任务,目标刺激是主要刺激。单个目标试验接受小波分析,以获得 delta(3 Hz)、theta(4-7 Hz)、alpha(8-12 Hz)、beta(13-30 Hz)和 gamma(30-50 Hz)频率的功率和相位锁定,时间窗口为 50 ms,中心位于目标 P3 峰值周围。当参与者接受苯丙胺时,P3 峰值周围的 delta 功率显着降低。Delta 相位锁定也降低了,但仅在分析针对 P3 峰值幅度的位置时才降低。相比之下,theta 功率和相位锁定不受苯丙胺影响。这些发现表明,增加儿茶酚胺活性可能是导致精神分裂症患者听觉 P3 delta 成分的功率和相位锁定降低的原因。有趣的是,苯丙胺显着增加了 P3 峰值周围的 gamma 功率。我们试图将这一发现与精神分裂症患者中发现的 gamma 改变联系起来。