Identification of thermo-receptor and elucidation of the functional mechanism

温度感受器的鉴定及其功能机制的阐明

• 批准号: 07680719
• 负责人: NAKAOKA Yasuo
• 金额: $ 1.47万
• 依托单位: Osaka University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1995
• 资助国家: 日本
• 起止时间: 1995 至 1996
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-07680719/
• 关键词: Sensory receptor; Temperature; Ca^<2+>; Prostaglandin; Paramecium; Mast cell; ATP receptor; イオン・チャネル

Paramecium cells respond to a temperature drop from the culture temperature and transiently depolarize the membrane, which triggers the directional changes in the swimming. We found that when the cells respond to the temperature drop, the intracellular Ca^<2+> transiently increased. The Ca^<2+> increase was restricted to the anterior part of the cell, corresponding to the sensitive part to the temperature drop. It was shown that the Ca^<2+> increase was caused by an influx of external Ca^<2+>.Some chemicals which seem to inhibit prostaglandin (PG) synthesis of Paramecium also inhibited the response to the temperature drop. On the other hand, when some PG were applied to the cell, the response to the temperature drop was recovered. The Paramecium cell has a sensitiviy to PG and showed a transient response when applied to the anterior part of the cell. These results suggest the possibility that the thermo-reception has some relationship to the prostaglandin receptor. Details of the relationship must be studied further.Rat mast cell line (RBL-2H3) was tested for the response to the temperature drop by the measurements of intracellular Ca^<2+>. When ATP was added in the external medium, the cells became to respond to the temperarure drop, and showed a transient increase in the intracellular Ca^<2+>. The Ca^<2+> increase was caused by the liberation from internal Ca^<2+> stores. Pharmacological analyzes showed that the ATP receptor has the sensitivity to the temperature drop. Activation mechanism of the ATP receptor remains to be elucidated further in the molecular level.

草履虫细胞对从培养温度下降的温度作出反应，并短暂地解除膜，这触发了游泳方向的变化。我们发现，当细胞对温度下降作出反应时，细胞内Ca^2+瞬时升高。Ca^<2+>的增加仅限于细胞的前部，对应于对温度下降敏感的部分。结果表明，草履虫体内Ca^<2 +>的增加是由外界Ca^<2+>内流引起的，一些抑制草履虫前列腺素（PG）合成的化合物也抑制了草履虫对降温的反应。另一方面，当将一些PG施加到细胞时，对温度下降的响应恢复。草履虫细胞对PG敏感，当PG作用于细胞前部时，表现出短暂的反应。这些结果提示热感受可能与前列腺素受体有关。通过测定大鼠肥大细胞系RBL-2 H3细胞内Ca^（2+）的含量，研究了RBL-2 H3细胞对降温的反应。当在体外培养液中加入ATP时，细胞对温度下降产生反应，并表现出胞内Ca^2+的短暂升高。Ca^<2+>的增加是由于从内部Ca^<2+>储存中释放出来所致.药理学分析表明，ATP受体对温度下降具有敏感性。ATP受体的激活机制还有待于在分子水平上进一步阐明。

项目成果

中岡保夫: "Possible mediation of G-proteins in cold-sensory transduction in Paramecium multimicronucleatum." J. Experimental Biology. 200. 1025-1030 (1997)

Yasuo Nakaoka：“多微核草履虫冷感觉转导中 G 蛋白的可能介导。实验生物学”200。1025-1030 (1997)

斉藤文仁: "The Photodynamic action of methylene blue on the ionchannels of Paramecium causes cell damage." Photochemistry and Photobiology. (印刷中). (1997)

Fumihito Saito：“亚甲基蓝对草履虫离子通道的光动力作用会导致细胞损伤。”（出版中）。

栗生 俊彦: "Cold-sensitive Ca^<2+> influx in Paramecium" J.Membrane Biology. 154. 163-167 (1996)

Toshihiko Kuryu：“草履虫中的冷敏感 Ca^<2+> 流入”J.Membrane Biology 154. 163-167 (1996)。

岡野聡: "Cloning of a novel ubiqitin-conjugating enzyme (E2) gene from the ciliated Paramecium tetraurelia." FEBS Letters. 391. 1-4 (1996)

Satoshi Okano：“从有纤毛的草履虫中克隆一种新型泛素结合酶 (E2) 基因。” FEBS Letters 391. 1-4 (1996)

Saitow, F., Nakaoka, Y.and Oosawa, Y.: "A calcium-activated, large conductance and non-selective cation channels in Paramecium cell." Biochem.Biophys.Acta.(in press). (1997)

Saitow, F.、Nakaoka, Y. 和 Oosawa, Y.：“草履虫细胞中的钙激活、大电导和非选择性阳离子通道。”