Melatonin inhibits nicotinic acetylcholine receptor functions in bovine chromaffin cells
10.11620/IJOB.2019.44.2.50
- Author:
Su Hyun JO
1
;
Seung Hyun LEE
;
Kyong Tai KIM
;
Se Young CHOI
Author Information
1. Department of Physiology, Institute of Bioscience and Biotechnology, BK21 Plus Graduate Program, Kangwon National University School of Medicine, Chuncheon 24341, Republic of Korea.
- Publication Type:Original Article
- Keywords:
Melatonin;
Nicotinic receptors;
Calcium signaling;
Neurotransmitter agents
- MeSH:
Calcium Signaling;
Central Nervous System;
Chromaffin Cells;
Circadian Rhythm;
Cytosol;
Dimethylphenylpiperazinium Iodide;
Melatonin;
Muscle Contraction;
Neurotransmitter Agents;
Nicotinic Agonists;
Norepinephrine;
Physiological Phenomena;
Receptors, Nicotinic;
Tooth
- From:International Journal of Oral Biology
2019;44(2):50-54
- CountryRepublic of Korea
- Language:English
-
Abstract:
Melatonin is a neurotransmitter that modulates various physiological phenomena including regulation and maintenance of the circadian rhythm. Nicotinic acetylcholine receptors (nAChRs) play an important role in oral functions including orofacial muscle contraction, salivary secretion, and tooth development. However, knowledge regarding physiological crosstalk between melatonin and nAChRs is limited. In the present study, the melatonin-mediated modulation of nAChR functions using bovine adrenal chromaffin cells, a representative model for the study of nAChRs, was investigated. Melatonin inhibited the nicotinic agonist dimethylphenylpiperazinium (DMPP) iodide-induced cytosolic free Ca²⁺ concentration ([Ca²⁺](i)) increase and norepinephrine secretion in a concentration-dependent manner. The inhibitory effect of melatonin on the DMPP-induced [Ca²⁺](i) increase was observed when the melatonin treatment was performed simultaneously with DMPP. The results indicate that melatonin inhibits nAChR functions in both peripheral and central nervous systems.
