Department of Psychiatry, University of North Carolina School of Medicine.
Nicotine Tob Res. 2018 Jun 7;20(7):897-902. doi: 10.1093/ntr/ntx177.
Prenatal nicotine exposure (PNE) from maternal cigarette smoking is linked to developmental deficits, including impaired auditory processing, language, generalized intelligence, attention, and sleep. Fetal brain undergoes massive growth, organization, and connectivity during gestation, making it particularly vulnerable to neurotoxic insult. Nicotine binds to nicotinic acetylcholine receptors, which are extensively involved in growth, connectivity, and function of developing neural circuitry and neurotransmitter systems. Thus, PNE may have long-term impact on neurobehavioral development. The purpose of this study was to compare the auditory K-complex, an event-related potential reflective of auditory gating, sleep preservation and memory consolidation during sleep, in infants with and without PNE and to relate these neural correlates to neurobehavioral development.
We compared brain responses to an auditory paired-click paradigm in 3- to 5-month-old infants during Stage 2 sleep, when the K-complex is best observed. We measured component amplitude and delta activity during the K-complex.
Infants with PNE demonstrated significantly smaller amplitude of the N550 component and reduced delta-band power within elicited K-complexes compared to nonexposed infants and also were less likely to orient with a head turn to a novel auditory stimulus (bell ring) when awake.
PNE may impair auditory sensory gating, which may contribute to disrupted sleep and to reduced auditory discrimination and learning, attention re-orienting, and/or arousal during wakefulness reported in other studies.
Links between PNE and reduced K-complex amplitude and delta power may represent altered cholinergic and GABAergic synaptic programming and possibly reflect early neural bases for PNE-linked disruptions in sleep quality and auditory processing. These may pose significant disadvantage for language acquisition, attention, and social interaction necessary for academic and social success.
母体吸烟导致的产前尼古丁暴露(PNE)与发育缺陷有关,包括听觉处理、语言、一般智力、注意力和睡眠受损。胎儿大脑在妊娠期经历大规模的生长、组织和连接,使其特别容易受到神经毒性的影响。尼古丁与烟碱型乙酰胆碱受体结合,这些受体广泛参与发育中的神经回路和神经递质系统的生长、连接和功能。因此,PNE 可能对神经行为发育产生长期影响。本研究的目的是比较有和没有 PNE 的婴儿的听觉 K 复合波,这是一种反映听觉门控的事件相关电位,以及睡眠期间的睡眠保存和记忆巩固,并将这些神经相关性与神经行为发育联系起来。
我们比较了 3 至 5 个月大的婴儿在 Stage 2 睡眠期间(K 复合波最容易观察到的阶段)对听觉成对点击范式的大脑反应。我们测量了 K 复合波期间的成分幅度和 delta 活动。
与未暴露于 PNE 的婴儿相比,PNE 婴儿的 N550 成分幅度明显较小,诱发的 K 复合波中的 delta 带功率降低,并且在清醒时更不可能通过转头对新的听觉刺激(铃声)做出反应。
PNE 可能会损害听觉感觉门控,这可能导致睡眠中断,并导致其他研究中报道的听觉辨别和学习、注意力重新定向和/或唤醒时的减少。
PNE 与 K 复合波幅度和 delta 功率降低之间的联系可能代表了胆碱能和 GABA 能突触编程的改变,并可能反映了 PNE 相关的睡眠质量和听觉处理中断的早期神经基础。这些可能对语言习得、注意力和社交互动造成重大不利影响,而这些是学术和社交成功所必需的。