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
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.