The Mouseion at the JAXlibrary

Title

Hyperactive somatostatin interneurons contribute to excitotoxicity in neurodegenerative disorders.

Authors

Wen Zhang
Lifeng Zhang
Bo Liang
David Schroeder, The Jackson LaboratoryFollow
Zhong-Wei Zhang, The Jackson LaboratoryFollow
Gregory A. Cox, The Jackson LaboratoryFollow
Yun Li
Da-Ting Lin

Document Type

Article

Publication Date

4-2016

JAX Source

Nat Neurosci 2016 Apr; 19(4):557-9.

PMID

26900927

Grant

1R21NS075382, Jackson Lab Startup Funds

Abstract

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.

Nat Neurosci 2016 Apr; 19(4):557-9.

Recommended Citation

Zhang, Wen; Zhang, Lifeng; Liang, Bo; Schroeder, David; Zhang, Zhong-Wei; Cox, Gregory A.; Li, Yun; and Lin, Da-Ting, "Hyperactive somatostatin interneurons contribute to excitotoxicity in neurodegenerative disorders." (2016). Faculty Research 2016. 87.
https://mouseion.jax.org/stfb2016/87