Neurobehavioural Toxicology and Chemosensation, IfADo - Leibniz Research Centre for Working Environment and Human Factors, Dortmund, Germany.
Neurotoxicology. 2012 Aug;33(4):911-24. doi: 10.1016/j.neuro.2011.10.002. Epub 2011 Oct 12.
The developing nervous system is particularly vulnerable to chemical insults. Exposure to chemicals can result in neurobehavioural alterations, and these have been used as sensitive readouts to assess neurotoxicity in animals and man. Deconstructing neurobehaviour into relevant cellular and molecular components may allow for detection of specific neurotoxic effects in cell-based systems, which in turn may allow an easier examination of neurotoxic pathways and modes of actions and eventually inform the regulatory assessment of chemicals with potential developmental neurotoxicity. Here, current developments towards these goals are reviewed. Imaging genetics (CB) provides new insights into the neurobiological correlates of cognitive function that are being used to delineate neurotoxic mechanisms. The gaps between in vivo neurobehaviour and real-time in vitro measurements of neuronal function are being bridged by ex vivo measurements of synaptic plasticity (RW). An example of solvent neurotoxicity demonstrates how an in vivo neurological defect can be linked via the N-methyl-d-aspartate (NMDA)-glutamate receptor as a common target to in vitro readouts (AB). Axonal and dendritic morphology in vitro proved to be good correlates of neuronal connectivity and neurobehaviour in animals exposed to polychlorinated biphenyls and organophosphorus pesticides (PJL). Similarly, chemically induced changes in neuronal morphology affected the formation of neuronal networks on structured surfaces. Such network formation may become an important readout for developmental neurotoxicity in vitro (CvT), especially when combined with human neurons derived from embryonic stem cells (ML). We envision that future in vitro test systems for developmental neurotoxicity will combine the above approaches with exposure information, and we suggest a strategy for test system development and cell-based risk assessment.
发育中的神经系统尤其容易受到化学物质的侵害。接触化学物质可能导致神经行为改变,这些改变已被用作评估动物和人类神经毒性的敏感指标。将神经行为分解为相关的细胞和分子成分,可以在基于细胞的系统中检测到特定的神经毒性效应,这反过来又可以更轻松地研究神经毒性途径和作用方式,并最终为具有潜在发育神经毒性的化学物质的监管评估提供信息。在这里,我们回顾了实现这些目标的最新进展。成像遗传学(CB)为认知功能的神经生物学相关性提供了新的见解,这些见解正被用于描绘神经毒性机制。通过对突触可塑性(RW)进行离体测量,正在弥合体内神经行为与实时体外神经元功能测量之间的差距。溶剂神经毒性的一个例子表明,如何通过 N-甲基-D-天冬氨酸(NMDA)-谷氨酸受体将体内神经学缺陷与体外读数(AB)联系起来。接触多氯联苯和有机磷农药的动物的体外轴突和树突形态学被证明是与动物神经连接和神经行为的良好相关性(PJL)。同样,化学诱导的神经元形态变化会影响在结构化表面上形成神经元网络。这种网络形成可能成为体外发育神经毒性的一个重要读数(CvT),尤其是当与源自胚胎干细胞的人类神经元结合使用时(ML)。我们设想,未来用于发育神经毒性的体外测试系统将结合上述方法和暴露信息,并提出了一种测试系统开发和基于细胞的风险评估策略。