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Int. J. Mol. Sci. 2015, 16(12), 28077-28086; doi:10.3390/ijms161226083

Critical Role of Endoplasmic Reticulum Stress in Cognitive Impairment Induced by Microcystin-LR

1,†
,
2,†
,
3,†
and
4,*
1
Department of Pharmacology, Hubei University of Science and Technology, Xianning 437100, China
2
Department of Pharmacy, The Central Hospital of Wuhan, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430014, China
3
Hubei Province Key Laboratory on Cardiovascular, Cerebrovascular, and Metabolic Disorders, Hubei University of Science and Technology, Xianning 437100, China
4
Fisheries College, Huazhong Agricultural University, Wuhan 430070, China
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Academic Editor: Masato Matsuoka
Received: 13 October 2015 / Revised: 16 November 2015 / Accepted: 17 November 2015 / Published: 25 November 2015
(This article belongs to the Special Issue Modulators of Endoplasmic Reticulum Stress)
View Full-Text   |   Download PDF [1807 KB, uploaded 25 November 2015]   |  

Abstract

Recent studies showed that cyanobacteria-derived microcystin-leucine-arginine (MCLR) can cause hippocampal pathological damage and trigger cognitive impairment; but the underlying mechanisms have not been well understood. The objective of the present study was to investigate the mechanism of MCLR-induced cognitive deficit; with a focus on endoplasmic reticulum (ER) stress. The Morris water maze test and electrophysiological study demonstrated that MCLR caused spatial memory injury in male Wistar rats; which could be inhibited by ER stress blocker; tauroursodeoxycholic acid (TUDCA). Meanwhile; real-time polymerase chain reaction (real-time PCR) and immunohistochemistry demonstrated that the expression level of the 78-kDa glucose-regulated protein (GRP78); C/EBP homologous protein (CHOP) and caspase 12 were significantly up-regulated. These effects were rescued by co-administration of TUDCA. In agreement with this; we also observed that treatment of rats with TUDCA blocked the alterations in ER ultrastructure and apoptotic cell death in CA1 neurons from rats exposed to MCLR. Taken together; the present results suggested that ER stress plays an important role in potential memory impairments in rats treated with MCLR; and amelioration of ER stress may serve as a novel strategy to alleviate damaged cognitive function triggered by MCLR. View Full-Text
Keywords: microcystin-LR; endoplasmic reticulum stress; cognitive impairment; tauroursodeoxycholic acid microcystin-LR; endoplasmic reticulum stress; cognitive impairment; tauroursodeoxycholic acid
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Cai, F.; Liu, J.; Li, C.; Wang, J. Critical Role of Endoplasmic Reticulum Stress in Cognitive Impairment Induced by Microcystin-LR. Int. J. Mol. Sci. 2015, 16, 28077-28086.

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