Imbalance between hippocampal projection cell and parvalbumin interneuron architecture increases epileptic susceptibility in mouse model of methyl CpG binding protein 2 duplication syndrome.
Junye GeShengjun XieJiamei DuanBiqing TianPengfei RenErling HuQiyi HuangHonghui MaoYuxin ZouQian ChenWenting WangPublished in: Epilepsia (2024)
Overexpression of MeCP2 may disrupt crucial signaling pathways, resulting in decreased dendritic complexity of PV interneurons and increased dendritic spine density of projection neurons. This reciprocal modulation of excitatory and inhibitory neuronal structures associated with MeCP2 implies its significance as a potential target in the development of epilepsy and offers a novel perspective on the co-occurrence of autism and epilepsy.
Keyphrases
- mouse model
- binding protein
- temporal lobe epilepsy
- signaling pathway
- image quality
- cerebral ischemia
- single cell
- autism spectrum disorder
- intellectual disability
- dna methylation
- spinal cord
- cell therapy
- cell proliferation
- high resolution
- case report
- transcription factor
- pi k akt
- stem cells
- computed tomography
- epithelial mesenchymal transition
- human health
- risk assessment
- mesenchymal stem cells
- brain injury
- oxidative stress
- magnetic resonance
- blood brain barrier
- induced apoptosis