Effects of (−)-Sesamin on Memory Deficits in MPTP-lesioned Mouse Model of Parkinson's Disease.
10.20307/nps.2016.22.4.246
- Author:
Ting Ting ZHAO
1
;
Keon Sung SHIN
;
Myung Koo LEE
Author Information
1. Department of Pharmacy and Research Center for Bioresource and Health, College of Pharmacy, Chungbuk National University, 1, Chungdae-ro, Seowon-gu, Cheongju 28644, Korea. myklee@chungbuk.ac.kr
- Publication Type:Original Article
- Keywords:
(−)-Sesamin;
MPTP-lesioned mouse model of Parkinson's disease;
Habit learning memory;
Spatial memory;
Dopaminergic neuron;
NMDA receptor
- MeSH:
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine;
3,4-Dihydroxyphenylacetic Acid;
Animals;
Carrier Proteins;
Dopamine;
Dopaminergic Neurons;
Homovanillic Acid;
Humans;
Learning;
Memory Disorders*;
Memory*;
Mice*;
N-Methylaspartate;
Norepinephrine;
Parkinson Disease*;
Phosphorylation;
Phosphotransferases;
Spatial Memory
- From:Natural Product Sciences
2016;22(4):246-251
- CountryRepublic of Korea
- Language:English
-
Abstract:
This study investigated the effects of (−)-sesamin on memory deficits in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned mouse model of Parkinson's disease (PD). MPTP lesion (30 mg/kg/day, 5 days) in mice showed memory deficits including habit learning memory and spatial memory. However, treatment with (−)-sesamin (25 and 50 mg/kg) for 21 days ameliorated memory deficits in MPTP-lesioned mouse model of PD: (−)-sesamin at both doses improved decreases in the retention latency time of the passive avoidance test and the levels of dopamine, norepinephrine, 3,4-dihydroxyphenylacetic acid, and homovanillic acid, improved the decreased transfer latency time of the elevated plus-maze test, reduced the increased expression of N-methyl-D-aspartate (NMDA) receptor, and increased the reduced phosphorylation of extracellular signal-regulated kinase (ERK1/2) and cyclic AMP-response element binding protein (CREB). These results suggest that (−)-sesamin has protective effects on both habit learning memory and spatial memory deficits via the dopaminergic neurons and NMDA receptor-ERK1/2-CREB system in MPTP-lesioned mouse model of PD, respectively. Therefore, (−)-sesamin may serve as an adjuvant phytonutrient for memory deficits in PD patients.
