Weng Octavia Yifang, Li Yun, Wang Lu-Yang
Program in Developmental and Stem Cell Biology, Sick Kids Research Institutes, Toronto, ON, Canada.
Program in Neuroscience and Mental Health, Sick Kids Research Institutes, Toronto, ON, Canada.
Front Mol Neurosci. 2022 Mar 10;15:810081. doi: 10.3389/fnmol.2022.810081. eCollection 2022.
Epilepsy is a neurological disorder that affects over 65 million people globally. It is characterized by periods of seizure activity of the brain as a result of excitation and inhibition (E/I) imbalance, which is regarded as the core underpinning of epileptic activity. Both gain- and loss-of-function (GOF and LOF) mutations of ion channels, synaptic proteins and signaling molecules along the mechanistic target of rapamycin (mTOR) pathway have been linked to this imbalance. The pathogenesis of epilepsy often has its roots in the early stage of brain development. It remains a major challenge to extrapolate the findings from many animal models carrying these GOF or LOF mutations to the understanding of disease mechanisms in the developing human brain. Recent advent of the human pluripotent stem cells (hPSCs) technology opens up a new avenue to recapitulate patient conditions and to identify druggable molecular targets. In the following review, we discuss the progress, challenges and prospects of employing hPSCs-derived neural cultures to study epilepsy. We propose a tentative working model to conceptualize the possible impact of these GOF and LOF mutations in ion channels and mTOR signaling molecules on the morphological and functional remodeling of intrinsic excitability, synaptic transmission and circuits, ultimately E/I imbalance and behavioral phenotypes in epilepsy.
癫痫是一种影响全球超过6500万人的神经系统疾病。其特征是由于兴奋与抑制(E/I)失衡导致大脑出现癫痫发作期,这种失衡被认为是癫痫活动的核心基础。雷帕霉素机制性靶点(mTOR)途径中的离子通道、突触蛋白和信号分子的功能获得性和功能丧失性(GOF和LOF)突变均与这种失衡有关。癫痫的发病机制通常源于大脑发育的早期阶段。将许多携带这些GOF或LOF突变的动物模型的研究结果外推至对发育中的人类大脑疾病机制的理解,仍然是一项重大挑战。人类多能干细胞(hPSCs)技术的最新出现为重现患者病情和识别可成药分子靶点开辟了一条新途径。在以下综述中,我们讨论了利用hPSCs衍生的神经培养物研究癫痫的进展、挑战和前景。我们提出了一个初步的工作模型,以概念化离子通道和mTOR信号分子中的这些GOF和LOF突变对内在兴奋性、突触传递和回路的形态和功能重塑的可能影响,最终导致癫痫中的E/I失衡和行为表型。