Vakhtin Andrei A, Kodituwakku Piyadasa W, Garcia Christopher M, Tesche Claudia D
Department of Psychology, University of New Mexico, Albuquerque, NM 87131, USA.
Department of Pediatrics, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.
Neuroimage Clin. 2015 Sep 18;9:392-400. doi: 10.1016/j.nicl.2015.09.005. eCollection 2015.
Dependent on maternal (e.g. genetic, age) and exposure (frequency, quantity, and timing) variables, the effects of prenatal alcohol exposure on the developing fetus are known to vary widely, producing a broad range of morphological anomalies and neurocognitive deficits in offspring, referred to as fetal alcohol spectrum disorders (FASD). Maternal drinking during pregnancy remains a leading risk factor for the development of intellectual disabilities in the US. While few functional findings exist today that shed light on the mechanisms responsible for the observed impairments in individuals with FASD, animal models consistently report deleterious effects of early alcohol exposure on GABA-ergic inhibitory pathways. The post-motor beta rebound (PMBR), a transient increase of 15-30 Hz beta power in the motor cortex that follows the termination of movement, has been implicated as a neural signature of GABA-ergic inhibitory activity. Further, PMBR has been shown to be a reliable predictor of age in adolescents. The present study sought to investigate any differences in the development of PMBR between FASD and control groups. Beta event-related de-synchronization (ERD) and movement-related gamma synchronization (MRGS), although not clearly linked to brain maturation, were also examined. Twenty-two participants with FASD and 22 age and sex-matched controls (12-22 years old) underwent magnetoencephalography scans while performing an auditory oddball task, which required a button press in response to select target stimuli. The data surrounding the button presses were localized to the participants' motor cortices, and the time courses from the locations of the maximally evoked PMBR were subjected to wavelet analyses. The subsequent analysis of PMBR, ERD, and MRGS revealed a significant interaction between group and age in their effects on PMBR. While age had a significant effect on PMBR in the controls, no simple effects of age were detected in the FASD group. The FASD group additionally displayed decreased overall ERD levels. No group or age effects on MRGS were detected. The described findings provide further evidence for broad impairments in inhibitory processes in adolescents with FASD, possibly related to aberrant development of GABA-ergic pathways.
取决于母体变量(如基因、年龄)和暴露变量(频率、数量和时间),已知产前酒精暴露对发育中的胎儿的影响差异很大,会在后代中产生广泛的形态异常和神经认知缺陷,即胎儿酒精谱系障碍(FASD)。在美国,孕期母亲饮酒仍然是导致智力残疾的主要风险因素。虽然目前很少有功能性研究结果能够揭示FASD患者所观察到的损伤的机制,但动物模型一致报告早期酒精暴露对γ-氨基丁酸(GABA)能抑制通路有有害影响。运动后β波反弹(PMBR)是运动终止后运动皮层中15 - 30赫兹β波功率的短暂增加,被认为是GABA能抑制活动的神经特征。此外,PMBR已被证明是青少年年龄的可靠预测指标。本研究旨在调查FASD组和对照组在PMBR发育方面的任何差异。还对β事件相关去同步化(ERD)和运动相关γ同步化(MRGS)进行了检查,尽管它们与大脑成熟没有明确联系。22名患有FASD的参与者以及22名年龄和性别匹配的对照组(12 - 22岁)在执行听觉oddball任务时接受了脑磁图扫描,该任务要求对选定的目标刺激进行按键响应。围绕按键的数据被定位到参与者的运动皮层,并对最大诱发PMBR位置的时间进程进行小波分析。随后对PMBR、ERD和MRGS的分析显示,组和年龄在对PMBR的影响上存在显著交互作用。虽然年龄对对照组的PMBR有显著影响,但在FASD组中未检测到年龄的简单效应。FASD组还显示出总体ERD水平降低。未检测到组或年龄对MRGS的影响。上述研究结果为FASD青少年抑制过程的广泛损伤提供了进一步证据,这可能与GABA能通路的异常发育有关。