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.

Volume

19

Issue

4

First Page

557

Last Page

559

ISSN

1546-1726

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 W, Zhang L, Liang B, Schroeder D, Zhang Z, Cox GA, Li Y, Lin D. Hyperactive somatostatin interneurons contribute to excitotoxicity in neurodegenerative disorders. Nat Neurosci 2016 Apr; 19(4):557-9.