Title
Hyperactive somatostatin interneurons contribute to excitotoxicity in neurodegenerative disorders.
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.