1998 Fiscal Year Final Research Report Summary
Effects of cyanide on a cation channel and catecholamine secretion
| Project/Area Number |
09680825
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
神経・脳内生理学
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| Research Institution | Fukuoka University |
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Principal Investigator |
INOUE Masumi Fukuoka Univ., Sch.of Med., Assoc.Prof., 医学部, 助教授 (40223276)
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| Co-Investigator(Kenkyū-buntansha) |
SAKAMOTO Yasuji Fukuoka Univ., Sch.of Med., Prof., 医学部, 教授 (30078761)
IMANAGA Issei Fukuoka Univ., Sch.of Med., Professor, 医学部, 教授 (40078613)
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| Project Period (FY) |
1997 – 1998
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| Keywords | chromaffin cell / anoxia / cation channel / muscarinic receptor / mitochondria / Ca / depolarization / ATP |
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| Research Abstract |
The whole-cell current in an isolated adrenal chromaffin cell of guinea pig was recorded with the Nystatin method. Application of 5 mM cyanide reversibly produced an inward current without a noticeable delay at negative membrane potentials. A similar current was elicited by exposure to hypoxic solution, which was saturated with 100% nitrogen gas and 0.5mM Na_2S_2O_4 was added to. The cyanide-induced current was not affected by replacement of sucrose with glucose. The results indicate that the effect of cyanide is due to chemical hypoxia The reversal potential of the cyanide current was -24 mV and the current voltage relationship had a negative slope region below -50mV.These characteristics of the cyanide current were similar to those of the muscarinic receptor-induced nonselective cation (NS) current. To elucidate whether exposure to cyanide evokes catecholamine secretion, catecholamine released from a single chromaffin cell was measured with amperometry. Application of cyanide and of muscarine both evoked catecholamine secretion, and this secretion was abolished by replacement of bath Ca^<2+> ions with Mg^<2+> or by application of the voltage-dependent Ca^<2+> channel blockers, Cd^<2+> and D-600. Muscarine and cyanide induced depolarization with a robust of firings and increased intracellular Ca^<2+> concentrations measured with the Ca^<2+> indicator Fluo-3 AM in a external Ca^<2+>-dependent manner. From these results, we conclude that muscarine and cyanide or chemical hypoxia evoke catecholamine secretion through depolarization and the subsequent activation of voltage-dependent Ca^<2+> channels and that the depolarization is at least in part due to activation of NS channels.
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