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J Pineal Res. 2015 Aug;59(1):24-37. doi: 10.1111/jpi.12235. Epub 2015 Apr 10.

Melatonin regulates the autophagic flux via activation of alpha-7 nicotinic acetylcholine receptors.

Author information

1
Biosafety Research Institute, College of Veterinary Medicine, Chonbuk National University, Jeonju, Korea.
2
Department of Bioactive Material Sciences and Research Center of Bioactive Materials, Chonbuk National University, Jeonju, Korea.

Abstract

Our previous study suggested that melatonin-mediated neuroprotective effects are related with the activation of autophagy. However, the mechanism of melatonin-mediated autophagic activation in prion-mediated mitochondrial damage is not reported. Alpha-7 nicotinic acetylcholine receptors (α7nAchR) is a member of nicotinic acetylcholine receptors, and α7nAchR activation regulates via melatonin. Thus, we hypothesized that melatonin-mediated neuroprotective effect related with to autophagy pathway as a result of α7nAchR regulation. Inactivation of α7nAchR inhibited melatonin-mediated autophagic activation and protective effect against prion-mediated mitochondrial neurotoxicity. Also, knockdown of ATG5 blocked the melatonin-mediated neuroprotection and did not influence to the activation of α7nAchR caused by melatonin. This report is the first study demonstrating that melatonin-mediated autophagic activation regulates via modulation of α7nAchR signals, and upregulation of α7nAchR signals induced by melatonin plays a pivotal role in neuroprotection of prion-mediated mitochondrial neurotoxicity. Our results suggested that regulator of α7 nAChR signals including melatonin may have used for neuroprotective strategies for the neurodegenerative disorders including prion diseases.

KEYWORDS:

alpha-7 nicotinic receptor; autophagy flux; melatonin; prion

PMID:
25808024
DOI:
10.1111/jpi.12235
[Indexed for MEDLINE]

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