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Updated: Dec 20, 2025
Assessment of Dendritic Arborization in the Dentate Gyrus of the Hippocampal Region in Mice
Published on: March 31, 2015
Dynamic alteration of dendrites and dendritic spines in the hippocampus and microglia in mouse brain tissues after
Lingling Xie1,2,3,4,5,6, Tianyi Li1,3,4,5,6, Xiaojie Song1,3,4,5,6
1Department of Neurology, Children's Hospital of Chongqing Medical University, Chongqing, China.
Purpose:
To study the alteration of microglial subtypes, the representative markers of microglia, and the morphology of dendrites and dendritic spines after acute status epilepticus (SE) and during recurrent seizures.
Methods:
A mouse kainate-induced SE model was used. Dendrites and dendritic spines of granule neurons in the dentate gyrus (DG) subregion and pyramidal neurons in the cornu ammonis (CA)1 and cornu ammonis (CA)3 subregions of the hippocampus were visualized by Golgi staining. Synaptic proteins were evaluated by Western blot analysis, and microglia and their markers were evaluated by flow cytometry.
Results:
Extensive partial spine loss was observed in the dendrites of granule and pyramidal cells in the acute and early chronic stages of SE. In terms of spine loss, the thin and mushroom types predominated. Accompanying the spine loss in these two stages, the proportion of M1 microglia increased significantly with high CX3CR1 expression and low CD200R expression. However, at the transiting stage, the proportion of M2 microglia was increased dramatically, and high expression levels of CXCR3 on all microglia and CD68 on M1 microglia were observed. Morris water maze tests revealed significant learning and memory impairment in the chronic phase of epilepsy.
Conclusion:
Dendritic spines in the hippocampus and microglia in the central nevus system are dynamically altered in epilepsy during the establishment and maintenance of spontaneous seizures. Microglia may contribute to the spine loss and related learning and memory impairment.
Insights
Epilepsy alters brain cell structures and immune cells, leading to spine loss and memory deficits. Microglia changes are linked to these impairments, offering insights into epilepsy progression.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Epilepsy is characterized by recurrent seizures, often leading to cognitive impairments.
- Microglia, the brain's resident immune cells, play a crucial role in central nervous system homeostasis and disease.
- Alterations in neuronal structure, specifically dendritic spines, are implicated in epilepsy-associated memory deficits.
Purpose of the Study:
- To investigate dynamic changes in microglial subtypes and their markers.
- To examine alterations in dendritic and dendritic spine morphology following status epilepticus (SE) and during recurrent seizures.
- To correlate these changes with learning and memory impairments in an epilepsy model.
Main Methods:
- A mouse model of kainate-induced status epilepticus (SE).
- Golgi staining to visualize dendritic and dendritic spine morphology in hippocampal neurons (DG, CA1, CA3).
- Flow cytometry to analyze microglial populations and marker expression (CX3CR1, CD200R, CXCR3, CD68).
- Western blot analysis for synaptic proteins.
- Morris water maze test for learning and memory assessment.
Main Results:
- Significant loss of dendritic spines (thin and mushroom types) in hippocampal neurons during acute and early chronic SE.
- Increased proportion of M1 microglia with high CX3CR1 and low CD200R expression in acute/early chronic stages.
- Shift towards M2 microglia during the transiting stage, with increased CXCR3 and CD68 expression on M1 microglia.
- Pronounced learning and memory impairment observed in the chronic phase of epilepsy.
Conclusions:
- Dendritic spines and microglia undergo dynamic alterations during the development and maintenance of epilepsy.
- Microglial activation and subtype shifts are associated with dendritic spine loss.
- These neuro-structural and cellular changes likely contribute to the learning and memory deficits characteristic of epilepsy.
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