Ugarte Gonzalo, Piña Ricardo, Contreras Darwin, Godoy Felipe, Rubio David, Rozas Carlos, Zeise Marc, Vidal Rodrigo, Escobar Jorge, Morales Bernardo
Laboratory of Neuroscience, Department of Biology, Faculty of Chemistry and Biology, University of Santiago of Chile, Santiago 9170022, Chile.
Department of Biology, Faculty of Sciences, Metropolitan University of Education Sciences, Santiago 7760197, Chile.
Biology (Basel). 2023 Sep 15;12(9):1241. doi: 10.3390/biology12091241.
Attention deficit-hyperactivity disorder (ADHD) is a neurodevelopmental disorder with high incidence in children and adolescents characterized by motor hyperactivity, impulsivity, and inattention. Magnetic resonance imaging (MRI) has revealed that neuroanatomical abnormalities such as the volume reduction in the neocortex and hippocampus are shared by several neuropsychiatric diseases such as schizophrenia, autism spectrum disorder and ADHD. Furthermore, the abnormal development and postnatal pruning of dendritic spines of neocortical neurons in schizophrenia, autism spectrum disorder and intellectual disability are well documented. Dendritic spines are dynamic structures exhibiting Hebbian and homeostatic plasticity that triggers intracellular cascades involving glutamate receptors, calcium influx and remodeling of the F-actin network. The long-term potentiation (LTP)-induced insertion of postsynaptic glutamate receptors is associated with the enlargement of spine heads and long-term depression (LTD) with spine shrinkage. Using a murine model of ADHD, a delay in dendritic spines' maturation in CA1 hippocampal neurons correlated with impaired working memory and hippocampal LTP has recently reported. The aim of this review is to summarize recent evidence that has emerged from studies focused on the neuroanatomical and genetic features found in ADHD patients as well as reports from animal models describing the molecular structure and remodeling of dendritic spines.
注意力缺陷多动障碍（ADHD）是一种在儿童和青少年中高发的神经发育障碍，其特征为多动、冲动和注意力不集中。磁共振成像（MRI）显示，精神分裂症、自闭症谱系障碍和ADHD等多种神经精神疾病都存在神经解剖学异常，如新皮层和海马体体积减小。此外，精神分裂症、自闭症谱系障碍和智力障碍中，新皮层神经元树突棘的异常发育和出生后修剪已有充分记录。树突棘是动态结构，表现出赫布可塑性和稳态可塑性，可触发涉及谷氨酸受体、钙内流和F-肌动蛋白网络重塑的细胞内级联反应。长时程增强（LTP）诱导的突触后谷氨酸受体插入与棘头增大有关，而长时程抑制（LTD）与棘收缩有关。最近有报道称，使用ADHD小鼠模型，CA1海马神经元树突棘成熟延迟与工作记忆受损和海马LTP受损相关。本综述的目的是总结近期研究证据，这些证据来自对ADHD患者神经解剖学和遗传特征的研究，以及动物模型中关于树突棘分子结构和重塑的报道。
