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
- image quality
- signaling pathway
- cerebral ischemia
- single cell
- autism spectrum disorder
- dna methylation
- cell therapy
- intellectual disability
- spinal cord
- cell proliferation
- case report
- transcription factor
- pi k akt
- human health
- risk assessment
- epithelial mesenchymal transition
- spinal cord injury
- mesenchymal stem cells
- bone marrow
- mass spectrometry
- blood brain barrier