| EFFECT OF OCTANOL, THE GAP JUNCTION BLOCKER, ON THE REGULATION OF FLUID SECRETION AND INTRACELLULAR CALCIUM CONCENTRATION IN SALIVARY ACINAR CELLS |
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| 흰쥐 악하선 세포에서 gap junction 봉쇄제인 octanol이 타액분비 및 세포내 $Ca^{2+}$ 수식 이미지 농도 조절에 미치는 영향 |
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이주석1, 서정택2, 이승일2, 이종갑1, 손흥규1 |
1연세대학교 치과대학 소아치과학교실
2연세대학교 치과대학 구강생물학교실 |
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| Abstract |
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From bacteria to mammalian cells, one of the most important mediators of intracellular signal transduction mechanisms which regulate a variety of intracellular processes is free calcium. In salivary acinar cells, elevation of intracellular calcium concentration ([Ca2+]i) is essential for the salivary secretion induced by parasympathetic stimulation. However, in addition to [Ca2+]i, gap junctions which couple individual cells electrically and chemically have also been reported to regulate enzyme secretion in pancreatic acinar cells. Since the plasma membrane of salivary acinar cells has a high density of gap junctions, and these cells are electrically and chemically coupled with each other, gap junctions may modulate the secretory function of salivary glands. In this respect, I planned to investigate the role of gap junctions in the modulation of salivary secretion and [Ca2+]i, using mandibular salivary glands of rats. In order to measure the salivary flow rate, fluid was collected from the cannulated duct of the isolated perfused rat mandibular glands at 2 min intervals. [Ca2+]i, was measured from the cells loaded with fura-2 by spectrofluorometry. The results obtained were as follows: 1. CCh-induced salivary secretion was reversibly inhibited by 1 mM octanol, a gap junction blocker. 2. CCh-induced increase in [Ca2+]i, was also reversed by the application of 1 mM octanol. 3. Octanol did not block the initial increase in [Ca2+]i caused by CCh, which suggested that the reduction of [Ca2+]i, caused by gap junction blockade was not resulted from the inhibition of Ca2+ release from intracellular Ca2+ stores. 4. Addition of octanol during stimulation with 1μM thapsigargin, a potent microsomal ATPase inhibitor, reduced [Ca2+]i, to the basal level. This suggested that inhibition of gap junction permeability closed plasma membrane Ca2+ channels. 5. 2,5-di-tert-butyl-1,4-benzohydroquinone (TBQ) generated [Ca2+]i oscillations resulting from periodic influx of Ca2+ via plasma membrane. The TBQ-induced [Ca2+]i oscillations were stopped by the application of 1mM octanol which implicated that gap junctions modulate the permeability of plasma membrane Ca2+ channels. 6. Glycyrrhetinic acid, another well known gap junction blocker, also inhibited CCh-induced salivary secretion from rat mandibular glands. These results suggested that gap junctions play an important role in the modulation of fluid secretion from the rat mandibular glands and this was probably due to the inhibition of Ca2+ influx through the plasma membrane Ca2+ channels. |
| Key Words:
gap junction, intracellular free calcium, octanol salivary secretion, octanol |
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