The changes in ionic permeability induced by the application of alpha-latrotoxin to NG108-15 neuroblastoma x glioma cells were examined using the nystatin perforated-patch technique for whole-cell recording. Complex single channel activity appeared in the plasmalemmas after delays that ranged from 1-20 min in Krebs' solution. The conductance of a channel fluctuated among at least three broad, approximately equispaced bands, the maximum conductance being about 300 pS, and the reversal potential approximately 0 mV. The channels were permeable to Na+, K+, Ca2+ and Mg2+, poorly permeable to glucosamineH+ and Cl-, and were blocked by La3+. The channels stayed fully open in Ca(2+)-free solutions with 4 mM Mg2+, in solutions with no divalent cations and in solutions with 2 mM Ca2+ and 96 mM Mg2+. They opened infrequently if both internal and external Cl- were replaced by glutamate-. If alpha-latrotoxin opened similar channels in nerve terminals, the flux of ions through them could account for the massive release of neurotransmitter induced by the toxin.
The changes in ionic permeability induced by the application of α-latrotoxin to NG108-15 neuroblastoma x glioma cells were examined using the nystatin perforated-patch technique for whole-cell recording. Complex single channel activity appeared in the plasmalemmas after delays that ranged from 1-20 min in Krebs' solution. The conductance of a channel fluctuated among at least three broad, approximately equispaced bands, the maximum conductance being about 300 pS, and the reversal potential approximately 0 mV. The channels were permeable to Na+, K+, Ca2+ and Mg2+, poorly permeable to glucosamineH+ and Cl-, and were blocked by La3+. The channels stayed fully open in Ca2+-free solutions with 4 m m Mg2+, in solutions with no divalent cations and in solutions with 2 m m Ca2+ and 96 m m Mg2+. They opened infrequently if both internal and external Cl- were replaced by glutamate-. If α-latrotoxin opened similar channels in nerve terminals, the flux of ions through them could account for the massive release of neurotransmitter induced by the toxin. © 1994 Springer-Verlag New York Inc.
α-Latrotoxin channels in neuroblastoma cells / Hurlbut, W. P.; Chieregatti, E.; Valtorta, F.; Haimann, C.. - In: THE JOURNAL OF MEMBRANE BIOLOGY. - ISSN 0022-2631. - 138:1(1994), pp. 91-102. [10.1007/BF00211072]
α-Latrotoxin channels in neuroblastoma cells
Valtorta F.Penultimo
;
1994-01-01
Abstract
The changes in ionic permeability induced by the application of α-latrotoxin to NG108-15 neuroblastoma x glioma cells were examined using the nystatin perforated-patch technique for whole-cell recording. Complex single channel activity appeared in the plasmalemmas after delays that ranged from 1-20 min in Krebs' solution. The conductance of a channel fluctuated among at least three broad, approximately equispaced bands, the maximum conductance being about 300 pS, and the reversal potential approximately 0 mV. The channels were permeable to Na+, K+, Ca2+ and Mg2+, poorly permeable to glucosamineH+ and Cl-, and were blocked by La3+. The channels stayed fully open in Ca2+-free solutions with 4 m m Mg2+, in solutions with no divalent cations and in solutions with 2 m m Ca2+ and 96 m m Mg2+. They opened infrequently if both internal and external Cl- were replaced by glutamate-. If α-latrotoxin opened similar channels in nerve terminals, the flux of ions through them could account for the massive release of neurotransmitter induced by the toxin. © 1994 Springer-Verlag New York Inc.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
