1993 Fiscal Year Final Research Report Summary
Mechanism of Ca^<2+> oscillation in salivaly gland acinar cells
| Project/Area Number |
04670044
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
General physiology
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| Research Institution | Tohoku University |
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Principal Investigator |
WAKUI Makoto Hirosaki University, School of Medicie, Department of Physiology, Professor, 医学部, 教授 (80108505)
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| Project Period (FY) |
1992 – 1993
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| Keywords | Ca^<2+> oscillation / Ca^<2+> wave / Ca^<2+> release / Ca^<2+> entry / inositol trisphosphate / IP_3 receptor / acetylcholine / exocrine gland cells |
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| Research Abstract |
Generation of the Ca^<2+> oscillation in response to secretagogues in exocrine gland acinar cells depends on two Ca^<2+> mobilizing mechanisms ; Ca^<2+> release from intracellular stores and Ca^<2+> entry from the extracellular space. To explore the precise mechanism of Ca^<2+> release, caged inositol trisphosphate (IP_3) was employed into the submandibular cells, and both Ca^<2+> activated Cl^- and K^+ currents were recorded. Photolytic transient release of a small amount of IP_3 caused only transient outward K^+ and inward Cl^- current, both of which were activated by Ca^<2+> released. On the other hand, release of relatively large amount of IP^3 caused additional Ca^<2+> activated delayd outward current. These indicate that Ca^<2+> releases from the IP_3-sensitive pools in an IP_3 concentration-dependen manner. Low concentrations of IP_3 release Ca^<2+> only locally, while high concentrations of IP_3 induce additinal Ca^<2+> release, which may be refect the Ca^<2+> wave progagation.
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The role of extracellular Ca^<2+> in the Ca^<2+> oscillation induced by acetylcholine (A Ch) was further studied by recording the Ca^<2+>-activated Cl^- currents. The higher the concentration of extracellular concentration of Ca^<2+>, the larger the amplitude of the repetitive Cl^- currents recorded. The Ca^<2+> oscillation ceased after removal of Ca^<2+> from the extracellular solution, and application of Ca^<2+> restored the Ca^<2+> oscillations. Application of Ca^<2+> to the extracellular solution after depletion of Ca^<2+> store by the first A Ch stimulation did not show any change in the membrane current in a condition without A Ch. However, the second stimulation with A Ch caused repetitive Ca^<2+>-activated Cl^- currents in a condition of Ca^<2+> being removed from the extracellular solution. These results indicate that the Ca^<2+> entry is essential to maintain the repetitive release of Ca^<2+>. Results further suggest that Ca^<2+> entering the cell is immediately taken up by Ca^<2+> stores and released by IP_3. Less
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