Department of Psychiatry, Maryland Psychiatric Research Center, University of Maryland School of Medicine, P.O. Box 21247, Baltimore, MD, 21228, USA.
Cogn Affect Behav Neurosci. 2020 Jun;20(3):658-668. doi: 10.3758/s13415-020-00794-5.
Nicotine increases the output of every major neurotransmitter. In previous studies designed to identify the secondary neurotransmitter systems mediating nicotine's attention-enhancing effects in a rat model, the β-adrenoceptor antagonist propranolol blocked these effects. The present study was designed to test whether this mechanism held true in humans, thus guiding development of novel nicotinic agonists for cognitive enhancement. Twenty-six nonsmokers completed a nicotine (7 mg/24 h transdermally) x propranolol (40 mg p.o., body weight-adjusted) interaction study. Over four test days, each participant received double-placebo, nicotine only, propranolol only, and nicotine plus propranolol in randomized sequence before cognitive testing. No drug effects were seen in a visuospatial attention task. In the Rapid Visual Information Processing Task, performed in two 15-min blocks, neither drug alone significantly affected hit rate, but both drugs combined acted synergistically to alleviate its decrement over time in the first block and displayed additive beneficial effects in the second. In a change detection task, propranolol enhanced accuracy and reduced reaction time independent of nicotine presence. Propranolol also enhanced subjective self-reports of vigor. Overall, the findings were contrary to those hypothesized. Propranolol displayed beneficial effects on cognition, especially on sustaining performance over time. β-adrenoceptor activation by nicotine-induced noradrenaline release appeared to limit performance-enhancing effects of nicotine, because they were unmasked by β-adrenoceptor antagonism. The results suggest that cognitive effects of changes in β-adrenoceptor tone are context-dependent; contrary to rodent paradigms, human cognitive paradigms require no physical orienting in space but prolonged periods of remaining stationary while sustaining predictable processing demands.
尼古丁增加了每一种主要神经递质的输出。在以前的研究中,为了确定介导尼古丁在大鼠模型中增强注意力的次要神经递质系统,β-肾上腺素受体拮抗剂普萘洛尔阻断了这些作用。本研究旨在测试这种机制是否适用于人类,从而指导新型尼古丁激动剂的开发,以增强认知能力。26 名不吸烟者完成了尼古丁(7mg/24h 经皮)×普萘洛尔(40mg po,按体重调整)相互作用研究。在四天的测试中,每个参与者都以随机顺序接受双安慰剂、尼古丁、普萘洛尔和尼古丁加普萘洛尔的治疗,然后进行认知测试。在视空间注意力任务中没有观察到药物作用。在快速视觉信息处理任务中,分为两个 15 分钟的部分进行,单独使用两种药物都没有显著影响击中率,但两种药物联合使用可以协同缓解第一部分的时间衰减,并在第二部分显示出附加的有益效果。在变化检测任务中,普萘洛尔在不依赖于尼古丁存在的情况下提高了准确性并降低了反应时间。普萘洛尔还增强了主观的活力自我报告。总的来说,这些发现与假设相反。普萘洛尔对认知功能有有益的影响,尤其是在长时间内维持表现。尼古丁诱导的去甲肾上腺素释放激活β-肾上腺素受体,似乎限制了尼古丁的增强作用,因为β-肾上腺素受体拮抗作用使这些作用显现出来。结果表明,β-肾上腺素受体张力变化的认知效应是依赖于背景的;与啮齿动物模型相反,人类认知模型不需要在空间中进行身体定向,而是需要长时间保持静止,同时维持可预测的处理需求。