Comparison of scopolamine-induced cognitive impairment responses in three different ICR stocks.
10.5625/lar.2018.34.4.317
- Author:
Woo Bin YOON
1
;
Hyeon Jun CHOI
;
Ji Eun KIM
;
Ji Won PARK
;
Mi Ju KANG
;
Su Ji BAE
;
Young Ju LEE
;
You Sang CHOI
;
Kil Soo KIM
;
Young Suk JUNG
;
Joon Yong CHO
;
Dae Youn HWANG
;
Hyun Keun SONG
Author Information
1. Department of Biomaterials Science, College of Natural Resources & Life Science/Life and Industry Convergence Research Institute, Pusan National University, Miryang, Korea. dyhwang@pusan.ac.kr
- Publication Type:Original Article
- Keywords:
ICR;
Korl:ICR;
scopolamine;
learning and memory
- MeSH:
Acetylcholinesterase;
Animals;
Brain Diseases;
Cognition Disorders*;
Cytokines;
DNA Nucleotidylexotransferase;
Humans;
Learning;
Memory;
Mice;
Mice, Inbred ICR;
Neurons;
Oxidative Stress;
Scopolamine Hydrobromide;
Superoxide Dismutase;
United Nations;
Water
- From:Laboratory Animal Research
2018;34(4):317-328
- CountryRepublic of Korea
- Language:English
-
Abstract:
Cognitive impairment responses are important research topics in the study of degenerative brain diseases as well as in understanding of human mental activities. To compare response to scopolamine (SPL)-induced cognitive impairment, we measured altered parameters for learning and memory ability, inflammatory response, oxidative stress, cholinergic dysfunction and neuronal cell damages, in Korl:ICR stock and two commercial breeder stocks (A:ICR and B:ICR) after relevant SPL exposure. In the water maze test, Korl:ICR showed no significant difference in SPL-induced learning and memory impairment compared to the two different ICRs, although escape latency was increased after SPL exposure. Although behavioral assessment using the manual avoidance test revealed reduced latency in all ICR mice after SPL treatment as compared to Vehicle, no differences were observed between the three ICR stocks. To determine cholinergic dysfunction induction by SPL exposure, activity of acetylcholinesterase (AChE) assessed in the three ICR stocks revealed no difference of acetylcholinesterase activity. Furthermore, low levels of superoxide dismutase (SOD) activity and high levels of inflammatory cytokines in SPL-treated group were maintained in all three ICR stocks, although some variations were observed between the SPLtreated groups. Neuronal cell damages induced by SPL showed similar response in all three ICR stocks, as assessed by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, Nissl staining analysis and expression analyses of apoptosis-related proteins. Thus, the results of this study provide strong evidence that Korl:ICR is similar to the other two ICR. Stocks in response to learning and memory capacity.
