Krishnan Manigandan, Mydeen Ayishal B, Nakhal Mohammed M, Ibrahim Marwa F, Jayaraj Richard L, Ljubisavljevic Milos R, Hamad Mohammad I K, Ismail Fatima Y
Department of Pediatrics, College of Medicine and Health Sciences, United Arab Emirates University, Al Ain, United Arab Emirates.
Department of Anatomy, College of Medicine and Health Sciences, United Arab Emirates University, Al Ain, United Arab Emirates.
Front Neuroanat. 2025 Jun 24;19:1580435. doi: 10.3389/fnana.2025.1580435. eCollection 2025.
Mutations in the methyl-CpG-binding protein-2 gene (), which cause Rett syndrome (RTT), disrupt neuronal activity; however, the impact of the loss-of-function on the cytoarchitecture of medial entorhinal cortex layer II (MECII) neurons-crucial for spatial memory and learning-remains poorly understood.
In this study, we utilized Golgi staining and neuron tracing in the 2 mouse model of RTT to investigate the pyramidal and stellate cell alterations in MECII.
Our findings revealed that pyramidal cells displayed a significant reduction in apical dendritic length, soma size, and spine density, while basal dendrites showed increased dendritic complexity and branching. On the other hand, stellate cells exhibited dendritic hypertrophy along with increased soma size, primary dendrites, and localized increase in dendritic intersections, despite an overall reduction in total dendritic length and spine density. These findings underscore the notion that loss-of-function can disrupt MECII pyramidal and stellate cell cytoarchitecture in a cell-type-specific manner, emphasizing its critical role in maintaining proper dendritic morphology in circuits, which is crucial for learning and memory.
甲基CpG结合蛋白2基因（）的突变会导致雷特综合征（RTT），破坏神经元活动；然而，功能丧失对内侧内嗅皮层II层（MECII）神经元细胞结构的影响——这对空间记忆和学习至关重要——仍然知之甚少。
在本研究中，我们利用雷特综合征的2小鼠模型进行高尔基染色和神经元追踪，以研究MECII中锥体细胞和星状细胞的改变。
我们的研究结果显示，锥体细胞的顶端树突长度、胞体大小和棘密度显著降低，而基底树突的树突复杂性和分支增加。另一方面，星状细胞表现出树突肥大，同时胞体大小、初级树突增加，树突交叉局部增加，尽管总树突长度和棘密度总体降低。这些发现强调了功能丧失可通过细胞类型特异性方式破坏MECII锥体细胞和星状细胞的细胞结构，强调了其在维持回路中适当树突形态方面的关键作用，而这对学习和记忆至关重要。
