Deficit in learning and memory of rats with chronic fluorosis correlates with the decreased expressions of M1 and M3 muscarinic acetylcholine receptors

To reveal the molecular mechanism of deficit in learning and memory induced by chronic fluorosis, the expression of muscarinic acetylcholine receptors (mAChRs) and oxidative stress were investigated. Sixty Sprague–Dawley (SD) rats were divided randomly into two groups (30 cases in each), i.e., the c...

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Veröffentlicht in:	Archives of toxicology 2015-11, Vol.89 (11), p.1981-1991
Hauptverfasser:	Dong, Yang-Ting, Wang, Ya, Wei, Na, Zhang, Qi-Fang, Guan, Zhi-Zhong
Format:	Artikel
Sprache:	eng
Schlagworte:	Animal cognition Animal memory Animals Biomedical and Life Sciences Biomedicine Chronic Disease Disease Models, Animal Environmental Health Female Fluoridation Fluorosis, Dental - complications Gene Expression Regulation Glutathione Peroxidase - metabolism Hydrogen Peroxide - metabolism Inorganic Compounds Male Malondialdehyde - metabolism Maze Learning Memory Disorders - etiology Occupational Medicine/Industrial Medicine Oxidative Stress Pharmacology/Toxicology Rats Rats, Sprague-Dawley Receptor, Muscarinic M1 - genetics Receptor, Muscarinic M3 - genetics RNA, Messenger - metabolism Rodents Superoxide Dismutase - metabolism Time Factors Toxicity
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Zusammenfassung:	To reveal the molecular mechanism of deficit in learning and memory induced by chronic fluorosis, the expression of muscarinic acetylcholine receptors (mAChRs) and oxidative stress were investigated. Sixty Sprague–Dawley (SD) rats were divided randomly into two groups (30 cases in each), i.e., the control group (
ISSN:	0340-5761 1432-0738
DOI:	10.1007/s00204-014-1408-2