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Journal of Neuroscience, Vol 12, 3372-3379, Copyright © 1992 by Society for Neuroscience
Metabolism of omega-conotoxin-sensitive voltage-operated calcium channels in human neuroblastoma cells: modulation by cell differentiation and anti-channel antibodies
M Passafaro, F Clementi and E Sher
Department of Medical Pharmacology, University of Milan, Italy.
The turnover of voltage-operated calcium channels was studied in two
different human neuroblastoma cell lines (IMR32 and SH-SY5Y) using
omega-conotoxin. The 125I-omega-conotoxin bound to surface channels was
internalized and degraded by the cells in a time- and temperature-
dependent manner. The radioactive degradation products released in the
medium were all trichloroacetic acid soluble and no longer recognized by
anti-omega-conotoxin antibodies. Altering the pH of intracellular
organelles with chloroquine and inhibiting lysosomal proteases with
leupeptin reduced 125I-omega-conotoxin degradation but had no effect on its
internalization. Postlabeling measurements showed that the rates of
125I-omega-conotoxin internalization and degradation were equal to the rate
of channel removal from the cell surface after protein synthesis
inhibition. The rate of removal of omega-conotoxin binding sites was
parallel to the rate of loss of functional channels, as measured by means
of the fura-2 technique. Drug-induced differentiation of human
neuroblastoma cells slowed down channel internalization and degradation
rates, leading to the known increased expression of plasma membrane calcium
channels in differentiated cells. On the other hand, both human (from
Lambert-Eaton myasthenic patients) and murine (from immunized mice)
anti-channel antibodies increased the rates of channel internalization and
degradation, leading to channel downregulation. The activity of presynaptic
calcium channels is already known to be acutely modulated by a number of
different agents (e.g., hormones and neurotransmitters); our studies
suggest that a different form of channel modulation (changes in the number
of channels due to interference with channel turnover) may be active over a
longer time scale in neurons.(ABSTRACT TRUNCATED AT 250 WORDS)
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