Int J Oral Biol.  2019 Jun;44(2):50-54. 10.11620/IJOB.2019.44.2.50.

Melatonin inhibits nicotinic acetylcholine receptor functions in bovine chromaffin cells

Affiliations
  • 1Department of Physiology, Institute of Bioscience and Biotechnology, BK21 Plus Graduate Program, Kangwon National University School of Medicine, Chuncheon 24341, Republic of Korea.
  • 2Department of Physiology, Dental Research Institute, Seoul National University School of Dentistry, Seoul 03080, Republic of Korea. sychoi@snu.ac.kr
  • 3Department of Life Sciences, Division of Integrative Bioscience and Biotechnology, Pohang University of Science and Technology, Pohang 37673, Republic of Korea.

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.

Keyword

Melatonin; Nicotinic receptors; Calcium signaling; Neurotransmitter agents
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