Melatonin inhibits nicotinic acetylcholine receptor functions in bovine chromaffin cells
2
조회
0
다운로드
0
인용
0
참고문헌
키워드
초록
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 Ca 2+ concentration ([Ca 2+ ] i ) increase and norepinephrine secretion in a concentration-dependent manner. The inhibitory effect of melatonin on the DMPP-induced [Ca 2+ ] 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.
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 Ca 2+ concentration ([Ca 2+ ] i ) increase and norepinephrine secretion in a concentration-dependent manner. The inhibitory effect of melatonin on the DMPP-induced [Ca 2+ ] 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.
참고문헌 (27)
- José Cipolla-Neto, "Melatonin as a Hormone: New Physiological and Clinical Insights", Endocrine Reviews, 39(6), pp.990~1028 (2018), The Endocrine Society[DOI]
- Rana Shafabakhsh, "Melatonin: A new inhibitor agent for cervical cancer treatment", Journal of Cellular Physiology, 234(12), pp.21670~21682 (2019), Wiley[DOI]
- T.-D. Kim, "Rhythmic control of AANAT translation by hnRNP Q in circadian melatonin production", Genes & Development, 21(7), pp.797~810 (2007), Cold Spring Harbor Laboratory[DOI]
- Rüdiger Hardeland, "Aging, Melatonin, and the Pro- and Anti-Inflammatory Networks", International Journal of Molecular Sciences, 20(5), pp.E1223~ (2019), MDPI AG[DOI]
- Anna Tarocco, "Melatonin as a master regulator of cell death and inflammation: molecular mechanisms and clinical implications for newborn care", Cell Death & Disease, 10(4), pp.317~ (2019), Springer Science and Business Media LLC[DOI]
- Bernard Bloem, "Cholinergic modulation of the medial prefrontal cortex: the role of nicotinic receptors in attention and regulation of neuronal activity", Frontiers in Neural Circuits, 8, pp.17~ (2014), Frontiers Media SA[DOI]
- Jin-Young Yoon, "Modulation of nicotinic receptor channels by adrenergic stimulation in rat pinealocytes", American Journal of Physiology-Cell Physiology, 306(8), pp.C726~C735 (2014), American Physiological Society[DOI]
- H Yawo, "Rectification of synaptic and acetylcholine currents in the mouse submandibular ganglion cells.", The Journal of Physiology, 417(1), pp.307~322 (1989), Wiley[DOI]
- Yoichiro Kashiwagi, "Nicotine up-regulates IL-8 expression in human gingival epithelial cells following stimulation with IL-1β or P. gingivalis lipopolysaccharide via nicotinic acetylcholine receptor signalling", Archives of Oral Biology, 57(5), pp.483~490 (2012), Elsevier BV[DOI]
- G. K. Johnson, "Interleukin-1 and interleukin-8 in nicotine- and lipopolysaccharide-exposed gingival keratinocyte cultures", Journal of Periodontal Research, 45, pp.583~588 (2010), Wiley[DOI]
- Amjad Almasri, "Nicotine and Lipopolysaccharide Affect Cytokine Expression From Gingival Fibroblasts", Journal of Periodontology, 78(3), pp.533~541 (2007), Wiley[DOI]
- Xiuping Wu, "Effects of tensile stress on the α1 nicotinic acetylcholine receptor expression in maxillofacial skeletal myocytes", Molecular and Cellular Biochemistry, 311(1-2), pp.51~56 (2008), Springer Science and Business Media LLC[DOI]
- Scott W. Rogers, "Nicotinic Receptor Alpha7 Expression during Tooth Morphogenesis Reveals Functional Pleiotropy", PLoS ONE, 7(5), pp.e36467~ (2012), Public Library of Science (PLoS)[DOI]
- E M Fenwick, "A patch-clamp study of bovine chromaffin cells and of their sensitivity to acetylcholine", The Journal of Physiology, 331(1), pp.577~597 (1982), Wiley[DOI]
- Higgins LS, "A desensitized form of neuronal acetylcholine receptor detected by 3H-nicotine binding on bovine adrenal chromaffin cells", J Neurosci, 8, pp.1436~1446 (1988)
- Cristina R. Artalejo, "Three types of Ca2+ channel trigger secretion with different efficacies in chromaffin cells", Nature, 367(6458), pp.72~76 (1994), Springer Science and Business Media LLC[DOI]
- Daniel L. Kilpatrick, "Stability of Bovine Adrenal Medulla Cells in Culture", Journal of Neurochemistry, 35(3), pp.679~692 (1980), Wiley[DOI]
- Kim KT, "Neomycin inhibits catecholamine secretion by blocking nicotinic acetylcholine receptors in bovine adrenal chromaffin cells", J Pharmacol Exp Ther, 288, pp.73~80 (1999)
- Keimin Lee, "Human salivary gland cells express bradykinin receptors that modulate the expression of proinflammatory cytokines", European Journal of Oral Sciences, 125(1), pp.18~27 (2017), Wiley[DOI]
- Grynkiewicz G, "A new generation of Ca2+ indicators with greatly improved fluorescence properties", J Biol Chem, 260, pp.3440~3450 (1985)
- Markus RP, "Melatonin modulation of presynaptic nicotinic acetylcholine receptors in the rat vas deferens", J Pharmacol Exp Ther, 279, pp.18~22 (1996)[DOI]
- Carlos Barajas-López, "Melatonin modulates cholinergic transmission by blocking nicotinic channels in the guinea-pig submucous plexus", European Journal of Pharmacology, 312(3), pp.319~325 (1996), Elsevier BV[DOI]
- Esther Parada, "The microglial α7-acetylcholine nicotinic receptor is a key element in promoting neuroprotection by inducing heme oxygenase-1 via nuclear factor erythroid2-related factor 2", Antioxidants & Redox Signaling, 19(11), pp.1135~1148 (2013), Mary Ann Liebert Inc[DOI]
- Oishi A, "Melatonin receptor signaling : impact of receptor oligomerization on receptor function", Int Rev Cell Mol Biol, 338, pp.59~77 (2018)[DOI]
- Pedro Lax, "Melatonin inhibits nicotinic currents in cultured rat cerebellar granule neurons", J Pineal Res, 44, pp.70~77 (2008), Wiley[DOI]
- Tae-Yong Choi, "Melatonin inhibits voltage-sensitive Ca2+ channel-mediated neurotransmitter release", Brain Research, 1557, pp.34~42 (2014), Elsevier BV[DOI]
- Regina P. Markus, "Is modulation of nicotinic acetylcholine receptors by melatonin relevant for therapy with cholinergic drugs?", Pharmacology & Therapeutics, 126(3), pp.251~262 (2010), Elsevier BV[DOI]
