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Chem Biol Interact. 2018 Apr 1;285:8-13. doi: 10.1016/j.cbi.2018.02.023. Epub 2018 Feb 21.

Melatonin attenuates scopolamine-induced cognitive impairment via protecting against demyelination through BDNF-TrkB signaling in the mouse dentate gyrus.

Author information

1
Department of Histology and Embryology, Institute of Neuroscience, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, PR China.
2
Department of Biomedical Science and Research Institute for Bioscience and Biotechnology, Hallym University, Chuncheon, Gangwon, 24252, Republic of Korea.
3
Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, Gangwon, 24341, Republic of Korea.
4
Department of Molecular and Cellular Biochemistry, School of Medicine, Kangwon National University, Chuncheon, Gangwon, 24252, Republic of Korea.
5
Department of Pharmacy, College of Pharmacy, Dankook University, Cheonan, Chungcheongnam, 31116, Republic of Korea.
6
Department of Anatomy and Cell Biology, College of Veterinary Medicine, Research Institute for Veterinary Science, Seoul National University, Seoul, 08826, Republic of Korea.
7
Department of Food Science and Nutrition, Hallym University, Chuncheon, Gangwon, 24252, Republic of Korea.
8
Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases, Yangzhou, Jiangsu, 225001, PR China.
9
Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, Gangwon, 24341, Republic of Korea. Electronic address: mhwon@kangwon.ac.kr.
10
Department of Biomedical Science and Research Institute for Bioscience and Biotechnology, Hallym University, Chuncheon, Gangwon, 24252, Republic of Korea. Electronic address: nqubik@hanmail.net.

Abstract

Animal models of scopolamine-induced amnesia are widely used to study underlying mechanisms and treatment of cognitive impairment in neurodegenerative diseases such as Alzheimer's disease (AD). Previous studies have identified that melatonin improves cognitive dysfunction in animal models. In this study, using a mouse model of scopolamine-induced amnesia, we assessed spatial and short-term memory functions for 4 weeks, investigated the expression of myelin-basic protein (MBP) in the dentate gyrus, and examined whether melatonin and scopolamine cotreatment could keep cognitive function and MBP expression. In addition, to study functions of melatonin for keeping cognitive function and MBP expression, we examined expressions of brain-derived neurotrophic factor (BDNF) and tropomycin receptor kinase B (TrkB) in the mouse dentate gyrus. Scopolamine (1 mg/kg) and melatonin (10 mg/kg) were intraperitoneally treated for 2 and 4 weeks. Two and 4 weeks after scopolamine treatment, mice showed significant cognitive impairment; however, melatonin and scopolamine cotreatment recovered cognitive impairment. Two and 4 weeks of scopolamine treatment, the density of MBP immunoreactive myelinated nerve fibers was significantly decreased in the dentate gyrus; however, scopolamine and melatonin cotreatment significantly increased the scopolamine-induced reduction of MBP expression in the dentate gyrus. Furthermore, the cotreatment of scopolamine and melatonin significantly increased the scopolamine-induced decrease of BDNF and TrKB immunoreactivity in the dentate gyrus. Taken together, our results indicate that melatonin treatment exerts anti-amnesic effect and restores the scopolamine-induced reduction of MBP expression through increasing BDNF and TrkB expressions in the mouse dentate gyrus.

KEYWORDS:

Immunohistochemistry; Morris water maze test; Myelinated nerve fibers; Neurotrophic factor; Passive avoidance test; Western blotting

PMID:
29476728
DOI:
10.1016/j.cbi.2018.02.023
[Indexed for MEDLINE]

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