Analysis with Ca2+ imaging and membrane potential measurement in neuroendocrine cells

神经内分泌细胞中的 Ca2 成像和膜电位测量分析

• 批准号: 07670071
• 负责人: SHIBUYA Izumi
• 金额: $ 0.38万
• 依托单位: University of Occupational and Environmental Health
• 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-07670071/
• 关键词: Ca^<2+> imaging; Patch clamp; supraoptic nucleus; GABA_B receptors; Prostaglandin E_2; PACAP; Ryanodine Ca^<2+> stores; non-selective cation channels; 非選択性陽イオンチャネル; Ryanodine感受性Ca^<2+>ストア; 視床下部; 視索上核; 神経内分泌; カルシウム画像解析; プロスタグランディン; サイトカイン

To elucidate the role and the regulatory mechanism of cytosolic Ca^<2+> concentrations ([Ca^<2+>]_i), we have measured [Ca^<2+>]_i and the membrane currents or membrane potentials in hypothalamic supraoptic nucleus (SON) neurons, adrenal chromaffin cells, and melanotrophs of the pituitary pars intermedia.The results of the study are following :1. The peptide PACAP increased [Ca^<2+>]_i in rat SON neurons by increasing Ca^<2+> entry. 2. In bovine adrenal chromaffin cells, PACAP induced both Ca^<2+> entry and Ca^<2+> release. 3. In rat melanotrophs, PACAP induced Ca^<2+> entry. 4. In bovine adrenal chromaffin cells, the peptide PAMP inhibited nicotinic currents and [Ca^<2+>]_i rises induced by nicotine. 5. GABA_B receptors were present in the presynaptic sites of the SON and inhibited both GABA and glutamate release. 6. Angiotensinll inhibited outwardly rectifying K^+ currents in SON neurons. 7. The AT1 antagonist losartan partially blocked electrically evoked synaptic currents in SON sl … More ices. 8. peptide adrenomedullin increased [Ca^<2+>]_i and modulated the firing of SON neurons. 9. GABA_B receptors were also present in the postsynaptic sites of the SON and inhibited voltage-gated Ca^<2+> currents. 10. Glutamate and its analogues increased [Ca^<2+>]_i and quisqualate and trans ACPD,agonists for metabotropic glutamate receptors, stimulated Ca^<2+> release in SON neurons. 11. Prostaglandin E_2 (PEGE_2) directly acted on SON neurons to induce [Ca^<2+>]_i rises and membrane depolarization, whereas interleukin 1beta did not have direct effect. 12. PGE_2 inhibited Ca^<2+> currents in rat melanotrophs through EP1, EP3, pertussis toxin sensitive G-proteins. 13. PACAP induced Ca^<2+> release from rynanodine-sensitive Ca^<2+> stores of bovine adrenal chromaffin cells. 14. There was a good correlation between spontaneous Ca^<2+> oscillations and phasic bursting in SON neurons. 15. Angiotensinll increased [Ca^<2+>]_i through losartan-sensitive AT1 receptors in rat subfornical organ neurons. Less

为了阐明胞浆Ca^<2+>浓度（[Ca^<2+>]_i）的作用及其调节机制，我们测量了下丘脑视上核（SON）神经元、肾上腺嗜铬细胞和垂体中间部促黑素细胞的[Ca^<2+>]_i和膜电流或膜电位。肽PACAP通过增加胞内Ca^<2 +>内流而增加SON神经元[Ca^<2+>]_i。2.在牛肾上腺嗜铬细胞中，PACAP同时诱导Ca^2+内流和Ca^2+释放。3.在大鼠黑素营养细胞中，PACAP可诱导Ca^2+内流。4.在牛肾上腺嗜铬细胞中，PAMP肽可抑制尼古丁诱导的烟碱电流和[Ca^<2+>] i升高。5. GABA_（B）受体位于SON的突触前部位，抑制GABA和谷氨酸的释放。6.血管紧张素II抑制SON神经元外向整流性K^+电流。7. AT1拮抗剂氯沙坦部分阻断SON sl电诱发的突触电流 ...更多信息 冰。8.肾上腺髓质素肽增加SON神经元[Ca^<2+>] i，调节SON神经元放电。9. GABA_B受体也存在于SON的突触后部位，并抑制电压门控Ca^2+电流。10.谷氨酸及其类似物增加视上核神经元[Ca^2+] i，促代谢型谷氨酸受体激动剂使君子酸和反式ACPD刺激视上核神经元Ca^2+释放。11.前列腺素E_2（PEGE_2）直接作用于SON神经元，引起[Ca^<2+>]_i升高和膜去极化，而白细胞介素1 β（IL 1 β）无直接作用。12. PGE_2通过EP1、EP3、百日咳毒素敏感G蛋白抑制大鼠黑素细胞Ca^<2+>电流。13. PACAP诱导牛肾上腺嗜铬细胞rynanodine敏感性钙库释放Ca^2+。14. SON神经元自发性Ca^<2+>振荡与时相性爆发之间存在良好的相关性。15.血管紧张素II通过氯沙坦敏感的AT 1受体增加大鼠穹窿下器神经元[Ca^<2+>]_i。少

项目成果

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Nagatomo,T.：“前肾髓质蛋白 N 末端 20 肽 (PAMP) 减少了牛肾上腺髓质细胞中尼古丁诱导的内向电流和 Ca^2 升高。”

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