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Bradykinin induces hyperpolarizations in rat glioma cells and in neuroblastoma X glioma hybrid cells.

作者信息

Reiser G, Hamprecht B

出版信息

Brain Res. 1982 May 6;239(1):191-9. doi: 10.1016/0006-8993(82)90841-1.

DOI:10.1016/0006-8993(82)90841-1
PMID:7093675
Abstract

The effect of the nonapeptide bradykinin on the membrane potential of permanent cell lines from neural origin was studied. A hyperpolarizing response of 10-30 s duration was produced when bradykinin was iontophoretically applied onto polyploid rat glioma cells (clone C6-4-2). Starting from the resting membrane potential the peak value of the hyperpolarizing response was reached within 0.5-1.5 s. Then the potential returned more slowly to the original value. The hyperpolarization was associated with an approximately 50% decrease in membrane resistance. Neither Na+ nor Cl- seemed to be important for the hyperpolarizing response, since bradykinin elicited similar hyperpolarizations in cells exposed to media in which Na+ or Cl- were replaced by choline or isethionate, respectively. Ca2+ fluxes are unlikely to be involved, since the addition of D600 did not affect the hyperpolarizations induced by bradykinin. However, a 10-fold increase in the concentration of K+ in the medium reduced the amplitude of the hyperpolarization by 40 mV. Thus, the hyperpolarization induced by bradykinin is associated with decrease in membrane resistance which is likely to be caused by an increased K+-conductance. The glioma cells showed a desensitization upon repeated application of bradykinin. However, the sensitivity of the cells to bradykinin was restored after 3-8 min of incubation in the absence of bradykinin. Since an antagonist of bradykinin is not known, the specificity of the action of bradykinin is difficult to assess. Nevertheless, the hyperpolarizing response to bradykinin appears to be specific insofar as other peptides, i.e. lutoliberin, thyroliberin, neurotensin, substance P and apamin, exerted no effect on the membrane potential of the glioma cells. Bradykinin-elicited hyperpolarizations with characteristics similar to those described above could also be demonstrated in neuroblastoma X glioma hybrid cells, but not in multinucleated fibroblast cells.

摘要

相似文献

1
Bradykinin induces hyperpolarizations in rat glioma cells and in neuroblastoma X glioma hybrid cells.
Brain Res. 1982 May 6;239(1):191-9. doi: 10.1016/0006-8993(82)90841-1.
2
Bradykinin-induced rapid breakdown of phosphatidylinositol 4,5-bisphosphate in neuroblastoma X glioma hybrid NG108-15 cells.缓激肽诱导神经母细胞瘤X胶质瘤杂交瘤NG108-15细胞中磷脂酰肌醇4,5-二磷酸的快速分解。
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3
Bradykinin induces inositol 1,4,5-trisphosphate-dependent hyperpolarization in K+ M-current-deficient hybrid NL308 cells: comparison with NG108-15 neuroblastoma x glioma hybrid cells.
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4
Bradykinin-activated transmembrane signals are coupled via No or Ni to production of inositol 1,4,5-trisphosphate, a second messenger in NG108-15 neuroblastoma-glioma hybrid cells.缓激肽激活的跨膜信号通过No或Ni与1,4,5-三磷酸肌醇的生成相偶联,1,4,5-三磷酸肌醇是NG108-15神经母细胞瘤-胶质瘤杂交细胞中的一种第二信使。
Proc Natl Acad Sci U S A. 1986 Feb;83(4):942-6. doi: 10.1073/pnas.83.4.942.
5
Bradykinin regulates the level of guanosine 3',5'-cyclic monophosphate (cyclic GMP) in neural cell lines.缓激肽调节神经细胞系中3',5'-环磷酸鸟苷(环鸟苷酸)的水平。
Brain Res. 1984 Jan 9;290(2):367-71. doi: 10.1016/0006-8993(84)90958-2.
6
The regulatory influence of bradykinin and inositol-1,4,5-trisphosphate on the membrane potential in neural cell lines.缓激肽和肌醇-1,4,5-三磷酸对神经细胞系膜电位的调节作用
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Sodium-channels in non-excitable glioma cells, shown by the influence of veratridine, scorpion toxin, and tetrodotoxin on membrane potential and on ion transport.藜芦碱、蝎毒素和河豚毒素对膜电位及离子转运的影响表明,非兴奋性胶质瘤细胞中存在钠通道。
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Transmitter responsiveness in two newly isolated clones of neuroblastoma X glioma hybrid.神经母细胞瘤X胶质瘤杂交瘤两个新分离克隆中的递质反应性
Brain Res. 1983 Jan 10;258(2):243-9. doi: 10.1016/0006-8993(83)91147-2.

引用本文的文献

1
Agonist-induced inhibition of inositol-trisphosphate-activated IK(Ca) in NG108-15 neuroblastoma hybrid cells.激动剂诱导的NG108-15神经母细胞瘤杂交细胞中肌醇三磷酸激活的IK(Ca)的抑制作用。
Pflugers Arch. 1993 Jan;422(4):364-70. doi: 10.1007/BF00374292.
2
Ca(2+)-dependent K+ channel activity in rat glioma cells induced by bradykinin stimulation and by inositol 1,4,5-trisphosphate injection.缓激肽刺激和注射肌醇1,4,5-三磷酸诱导大鼠胶质瘤细胞中钙依赖性钾通道活性。
Cell Mol Neurobiol. 1993 Dec;13(6):615-24. doi: 10.1007/BF00711561.
3
Sodium-channels in non-excitable glioma cells, shown by the influence of veratridine, scorpion toxin, and tetrodotoxin on membrane potential and on ion transport.
藜芦碱、蝎毒素和河豚毒素对膜电位及离子转运的影响表明,非兴奋性胶质瘤细胞中存在钠通道。
Pflugers Arch. 1983 Jun 1;397(4):260-4. doi: 10.1007/BF00580258.
4
Bradykinin causes a transient rise of intracellular Ca2+-activity in cultured neural cells.
Pflugers Arch. 1985 Oct;405(3):260-4. doi: 10.1007/BF00582570.
5
Effects of bradykinin on electrical properties of Madin-Darby canine kidney epithelioid cells.缓激肽对犬肾Madin-Darby上皮样细胞电特性的影响。
Pflugers Arch. 1987 Apr;408(4):408-13. doi: 10.1007/BF00581137.
6
Inositol 1,4,5-trisphosphate and diacylglycerol mimic bradykinin effects on mouse neuroblastoma x rat glioma hybrid cells.肌醇1,4,5-三磷酸和二酰基甘油模拟缓激肽对小鼠神经母细胞瘤x大鼠胶质瘤杂交细胞的作用。
J Physiol. 1988 Mar;397:185-207. doi: 10.1113/jphysiol.1988.sp016995.
7
Bradykinin-activated transmembrane signals are coupled via No or Ni to production of inositol 1,4,5-trisphosphate, a second messenger in NG108-15 neuroblastoma-glioma hybrid cells.缓激肽激活的跨膜信号通过No或Ni与1,4,5-三磷酸肌醇的生成相偶联,1,4,5-三磷酸肌醇是NG108-15神经母细胞瘤-胶质瘤杂交细胞中的一种第二信使。
Proc Natl Acad Sci U S A. 1986 Feb;83(4):942-6. doi: 10.1073/pnas.83.4.942.
8
Acetylcholine release by bradykinin, inositol 1,4,5-trisphosphate and phorbol dibutyrate in rodent neuroblastoma cells.缓激肽、肌醇1,4,5 -三磷酸酯和佛波醇二丁酸酯在啮齿动物神经母细胞瘤细胞中诱导乙酰胆碱释放的研究
J Physiol. 1988 Mar;397:209-22. doi: 10.1113/jphysiol.1988.sp016996.
9
Membrane current responses of NG108-15 mouse neuroblastoma x rat glioma hybrid cells to bradykinin.NG108-15小鼠神经母细胞瘤x大鼠胶质瘤杂交细胞对缓激肽的膜电流反应。
J Physiol. 1988 Mar;397:167-84. doi: 10.1113/jphysiol.1988.sp016994.
10
A transient outward current in NG108-15 neuroblastoma x glioma hybrid cells.NG108-15神经母细胞瘤x胶质瘤杂交细胞中的瞬时外向电流。
Pflugers Arch. 1990 Apr;416(1-2):130-7. doi: 10.1007/BF00370234.