Temporal and spatial changes of α7nAChR and nNOS in cerebral cortex and hippocampus of Aβ-induced cognitive dysfunction rats.
- Author:
Yan-Li WANG
1
;
Li-Xia LIU
2
;
Shao-Hu WANG
2
;
Wen-Xiu QI
3
Author Information
1. Basic Medical College, Shanxi Medical University, Taiyuan 030001, China.
2. Department of Physiology, Fenyang College of Shanxi Medical University, Fenyang 032200, China.
3. Department of Physiology, Fenyang College of Shanxi Medical University, Fenyang 032200, China. fycqwx@163.com.
- Publication Type:Journal Article
- MeSH:
Amyloid beta-Peptides;
Animals;
Cerebral Cortex;
Cognitive Dysfunction;
Hippocampus;
Learning;
Memory;
Nitric Oxide Synthase Type I;
Rats;
Rats, Sprague-Dawley;
alpha7 Nicotinic Acetylcholine Receptor
- From:
Acta Physiologica Sinica
2016;68(6):775-782
- CountryChina
- Language:Chinese
-
Abstract:
The present study was to explore the temporal and spatial distributions and variations of α7 nicotinic acetylcholine receptor (α7nAChR) and neuronal nitric oxide synthetase (nNOS) in cerebral cortex and hippocampus of Aβ-induced cognitive dysfunction rats. Sixty Sprague-Dawley (SD) rats were randomly divided into six groups. Three experimental groups were intracerebroventricularly (i.c.v.) injected with condensed-amyloid beta peptides 1-42 (Aβ, 2.5 µg/µL, 4 µL) and were observed on day 7 (7 d Aβ group), day 14 (14 d Aβ group) and day 21 (21 d Aβ group), respectively. Three control groups were i.c.v. injected with equivalent volume of normal saline and observed at the same time points as the experimental groups. The learning and memory abilities of rats were tested with Y-maze; the locations and protein expression levels of α7nAChR and nNOS in cerebral cortex and hippocampal CA1, CA3, DG regions were measured by immunohistochemistry and Western blot, respectively. The result showed that, compared with the control groups, the three experimental groups exhibited decreased learning and memory behavioral abilities, and down-regulated expressions of nNOS and α7nAChR in prefrontal cortex and hippocampal regions, especially in superficial layer of prefrontal cortex and hippocampal CA3 region. Comparisons among the three experimental groups showed that the inhibitory effects of Aβ on the abilities of learning and memory and the expressions of α7nAChR and nNOS in prefrontal cortex and hippocampus were time dependent. The results suggest that the coincident declines of α7nAChR and nNOS in prefrontal cortex and hippocampus may be the foundations of the cognitive dysfunction.
