Dendritic Cell Factor 1-Knockout Results in Visual Deficit Through the GABA System in Mouse Primary Visual Cortex.
10.1007/s12264-018-0211-0
- Author:
Jieyun SHI
1
;
Qian LI
1
;
Tieqiao WEN
2
Author Information
1. Laboratory of Molecular Neural Biology, School of Life Sciences, Shanghai University, 333 Nanchen Road, Shanghai, 200444, China.
2. Laboratory of Molecular Neural Biology, School of Life Sciences, Shanghai University, 333 Nanchen Road, Shanghai, 200444, China. wtq@shu.edu.cn.
- Publication Type:Journal Article
- Keywords:
DCF1;
GABA;
GAD67;
Sight
- MeSH:
Animals;
Brain Waves;
genetics;
Disease Models, Animal;
Electroencephalography;
Gene Expression Regulation;
drug effects;
genetics;
Geniculate Bodies;
drug effects;
metabolism;
Ginkgolides;
therapeutic use;
Glutamate Decarboxylase;
metabolism;
Lactones;
therapeutic use;
Membrane Proteins;
deficiency;
genetics;
Mice;
Mice, Inbred C57BL;
Mice, Knockout;
Nerve Tissue Proteins;
deficiency;
genetics;
Photic Stimulation;
Proto-Oncogene Proteins c-fos;
metabolism;
Vision Disorders;
drug therapy;
genetics;
pathology;
physiopathology;
Visual Cortex;
metabolism;
pathology;
gamma-Aminobutyric Acid;
metabolism
- From:
Neuroscience Bulletin
2018;34(3):465-475
- CountryChina
- Language:English
-
Abstract:
The visual system plays an important role in our daily life. In this study, we found that loss of dendritic cell factor 1 (DCF1) in the primary visual cortex (V1) caused a sight deficit in mice and induced an abnormal increase in glutamic acid decarboxylase 67, an enzyme that catalyzes the decarboxylation of glutamate to gamma aminobutyric acid and CO, particularly in layer 5. In vivo electrophysiological recordings confirmed a decrease in delta, theta, and beta oscillation power in DCF1-knockout mice. This study presents a previously unknown function of DCF1 in V1, suggests an unknown contact between DCF1 and GABA systems, and provides insight into the mechanism and treatment of visual deficits.
