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Publication : Hyperactive somatostatin interneurons contribute to excitotoxicity in neurodegenerative disorders.

First Author  Zhang W Year  2016
Journal  Nat Neurosci Volume  19
Issue  4 Pages  557-559
PubMed ID  26900927 Mgi Jnum  J:234511
Mgi Id  MGI:5790147 Doi  10.1038/nn.4257
Citation  Zhang W, et al. (2016) Hyperactive somatostatin interneurons contribute to excitotoxicity in neurodegenerative disorders. Nat Neurosci 19(4):557-9
abstractText  Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are overlapping neurodegenerative disorders whose pathogenesis remains largely unknown. Using TDP-43(A315T) mice, an ALS and FTD model with marked cortical pathology, we found that hyperactive somatostatin interneurons disinhibited layer 5 pyramidal neurons (L5-PNs) and contributed to their excitotoxicity. Focal ablation of somatostatin interneurons efficiently restored normal excitability of L5-PNs and alleviated neurodegeneration, suggesting a new therapeutic target for ALS and FTD.
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