CHOLINERGIC RESPONSES IN CLONED HUMAN TE671/RD TUMOR-CELLS

被引:14
作者
GRASSI, F
GIOVANNELLI, A
FUCILE, S
MATTEI, E
EUSEBI, F
机构
[1] UNIV AQUILA,DIPARTIMENTO MED SPERIMENTALE,LAQUILA,ITALY
[2] INST REGINA ELENA STUDIO & CURA TUMORI,BIOFIS LAB,I-00158 ROME,ITALY
[3] CNR,IST TECNOL BIOMED,ROME,ITALY
来源
PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY | 1993年 / 425卷 / 1-2期
关键词
NICOTINIC ACETYLCHOLINE RECEPTOR; MUSCARINIC ACETYLCHOLINE RECEPTOR; TE671/RD CELL LINE; INOSITOL 1,4,5-TRISPHOSPHATE; PHOSPHOINOSITIDE TURNOVER; CA2+ IMAGING;
D O I
10.1007/BF00374511
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The cholinergic responses of the human tumour cell line TE671/RD were examined using digital Ca2+ imaging fluorescence microscopy and patch-clamp measurements. In response to stimulation of the muscarinic acetylcholine (ACh) receptor (mAChR), the intracellular concentration of Ca2+ ([Ca2+],) rose about twofold, in parallel with inositol 1,4,5-trisphosphate accumulation, measured by chromatographic techniques. By contrast, there was no increment of [Ca2+], upon stimulation of the nicotinic ACh receptor (nAChR), nor after caffeine application. Electrophysiological experiments showed that TE671/RD cells lack functional voltage-activated Ca2+ channels. The stimulation of the nAChR induced transient whole-cell currents (I-ACh). Little or no current was detected in isotonic extracellular Ca2+, with Cs+ in the patch pipette. Cell pretreatment with muscarine reduced I-ACh by about 20%, without consistent modifications of current kinetics. Muscarine applied to the extra-patch membrane under the cell-attached configuration had no obvious effect on ACh-evoked unitary events. In conclusion, in human TE671/RD cells, muscarinic stimulation increases [Ca2+](i), while nicotinic stimulation does not. In addition, the nAChR exhibits peculiar ion permeability properties and is not functionally regulated by the breakdown of phosphoinositides.
引用
收藏
页码:117 / 125
页数:9
相关论文
共 33 条
  • [1] THE PERMEABILITY OF ENDPLATE CHANNELS TO MONO-VALENT AND DIVALENT METAL-CATIONS
    ADAMS, DJ
    DWYER, TM
    HILLE, B
    [J]. JOURNAL OF GENERAL PHYSIOLOGY, 1980, 75 (05) : 493 - 510
  • [2] BENCHERIF M, 1991, J PHARMACOL EXP THER, V257, P946
  • [3] INOSITOL PHOSPHATES AND CELL SIGNALING
    BERRIDGE, MJ
    IRVINE, RF
    [J]. NATURE, 1989, 341 (6239) : 197 - 205
  • [4] CALCIUM CONDUCTANCE OF ACETYLCHOLINE-INDUCED ENDPLATE CHANNELS
    BREGESTOVSKI, PD
    MILEDI, R
    PARKER, I
    [J]. NATURE, 1979, 279 (5714) : 638 - 639
  • [5] Caratsch C G, 1992, Ion Channels, V3, P177
  • [6] CELL IDENTITY RESOLVED
    CHEN, TR
    DOROTINSKY, C
    MACY, M
    HAY, R
    [J]. NATURE, 1989, 340 (6229) : 106 - 106
  • [7] MUTATIONS IN M2 ALTER THE SELECTIVITY OF THE MOUSE NICOTINIC ACETYLCHOLINE-RECEPTOR FOR ORGANIC AND ALKALI-METAL CATIONS
    COHEN, BN
    LABARCA, C
    DAVIDSON, N
    LESTER, HA
    [J]. JOURNAL OF GENERAL PHYSIOLOGY, 1992, 100 (03) : 373 - 400
  • [8] DECKER ER, 1990, J NEUROSCI, V10, P3413
  • [9] INACTIVATION OF HUMAN SODIUM-CHANNELS AND THE EFFECT OF TOCAINIDE
    FAKLER, B
    RUPPERSBERG, JP
    SPITTELMEISTER, W
    RUDEL, R
    [J]. PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY, 1990, 415 (06): : 693 - 700
  • [10] ACETYLCHOLINE INDUCES VOLTAGE-INDEPENDENT INCREASE OF CYTOSOLIC CALCIUM IN MOUSE MYOTUBES
    GIOVANELLI, A
    GRASSI, F
    MATTEI, E
    MILEO, AM
    EUSEBI, F
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1991, 88 (22) : 10069 - 10073