ArticleActa neuropathologica2024
Impaired GABAergic regulation and developmental immaturity in interneurons derived from the medial ganglionic eminence in the tuberous sclerosis complex.
Article in Acta neuropathologica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Molecular Basis of GABA Aminotransferase Inhibition in Epilepsy: Structure, Mechanisms, and Drug Development.Current issues in molecular biology · 2025Review
- Cell-cell communication dysregulation in tuberous sclerosis complex cortical tubers and focal cortical dysplasia.Acta neuropathologica communications · 2025Article
- Single nuclei transcriptomics reveals cellular diversity in TSC subependymal giant cell astrocytomas.iScience · 2025Article
- Transcriptional Consequences of MeCP2 Knockdown and Overexpression in Mouse Primary Cortical Neurons.International journal of molecular sciences · 2025Article
- Article
- Metabolic syndrome in patients with schizophrenia: Underlying mechanisms and therapeutic approaches (Review).Molecular medicine reports · 2025Review
- Targeting ApoE-KCC2 Signaling Rescues GABAergic Synaptic Dysfunction and Depression-like Behaviors in Mice.Research (Washington, D.C.) · 2025Article
- A novel de novo GABRA2 gene missense variant causing developmental epileptic encephalopathy in a Chinese patient.Annals of clinical and translational neurology · 2025Article
- Focal postnatal deletion ofFrontiers in molecular neuroscience · 2025Article
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Authors and funding
16 authors.
Funding
Abstract
GABAergic interneurons play a critical role in maintaining neural circuit balance, excitation-inhibition regulation, and cognitive function modulation. In tuberous sclerosis complex (TSC), GABAergic neuron dysfunction contributes to disrupted network activity and associated neurological symptoms, assumingly in a cell type-specific manner. This GABAergic centric study focuses on identifying specific interneuron subpopulations within TSC, emphasizing the unique characteristics of medial ganglionic eminence (MGE)- and caudal ganglionic eminence (CGE)-derived interneurons. Using single-nuclei RNA sequencing in TSC patient material, we identify somatostatin-expressing (SST+) interneurons as a unique and immature subpopulation in TSC. The disrupted maturation of SST+ interneurons may undergo an incomplete switch from excitatory to inhibitory GABAergic signaling during development, resulting in reduced inhibitory properties. Notably, this study reveals markers of immaturity specifically in SST+ interneurons, including an abnormal NKCC1/KCC2 ratio, indicating an imbalance in chloride homeostasis crucial for the postsynaptic consequences of GABAergic signaling as well as the downregulation of GABA
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