Dietary restriction enhancesγ-aminobutyric acid and brain derived neurotrophic factor expression in the visual cortex of the cat
10.3969/j.issn.0529-1356.2014.03.002
- VernacularTitle:节制饮食增强猫视皮层γ-氨基丁酸和脑源性神经营养因子的表达
- Author:
Cuiyun CHEN
;
Hui ZHU
;
Peng LI
;
Qingyan SUN
;
Tianmiao HUA
- Publication Type:Journal Article
- Keywords:
Dietary restriction;
γ-Aminobutyric acid;
Brain derived neurotrophic factor;
Visual cortex;
Immunohistochemistry;
Cat
- From:
Acta Anatomica Sinica
2014;(3):304-309
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the effect of DR on the expression of inhibitory neurotransmitter ,γ-aminobutyric acid ( GABA) and brain derived neurotrophic factor ( BDNF) in the primary visual cortex of young cats .Methods Totally 6 cats were wsed in this study . Nissl staining was used for cortical layer identification and cell counting . Immunohistochemical techniques were utilized to label GABA-and BDNF-positive neurons .Sections were observed under an Olympus light microscope and photographed with a digital camera .The cell density and absorbance of immunoreactivity were measured with Image-Pro Express 6.0 softwares .Results Our results showed that the mean density of Nissl-stained neurons in the primary visual cortex ( V1) of the DR group showed no significant difference from that of the control group . However , the mean density of GABA-immunoreactive neurons in each cortical layer of V 1 in DR cats was significantly higher than that in control cats .The mean immunoreactive intensity of GABA-positive neurons , as indicated by the average absorbance , increased significantly in DR cats relative to control ones . Accompanied with the elevation of GABA expression, DR enhanced BDNF expression in V1, as indicated by an increased mean density of BDNF-positive neurons and BDNF-immunoreactive average absorbance in DR cats relative to controls .Conclusion These results indicate that dietary restriction leads to a concurrent expression upregulation of GABA and BDNF , which may likely compensate for brain functional degradation during senescence and thus delay aging process .
