Premium
Characteristics of the K‐252a‐induced increase in calcium uptake in PC12 cells
Author(s) -
Nikodijevic B.,
Aschkenasy M.,
Dickens G.,
Lachance C.,
Guroff Gordon
Publication year - 1995
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490400408
Subject(s) - calcium , nerve growth factor , t type calcium channel , voltage dependent calcium channel , receptor , microbiology and biotechnology , chemistry , endocrinology , biophysics , medicine , biology , pharmacology , biochemistry
K‐252a treatment produced a 30–50% increase in the uptake of radioactive calcium by PC12 cells within 3–4 minutes. The increase in uptake was partially blocked by inhibitors of voltage‐operated calcium channels, such as nifedipine, but not by inhibitors of receptor‐operated calcium channels, such as nickel or suramin. Introduction of phosphatase 2A into the cells completely blocked the effect of K‐252a. Longterm treatment of the cells with either K‐252a or with nerve growth factor blocked the subsequent actions of either K‐252a or nerve growth factor on calcium uptake, but neither altered the subsequent action of the L‐channel agonist Bay K 8644 on calcium uptake. Calcium uptake was not stimulated by K‐252a in PC12nnr, cells that have little or no high‐affinity nerve growth factor receptors; cells expressing increased levels of high‐affinity nerve growth factor receptors showed a response to K‐252a comparable to that seen in parent PC12. The data suggest that the increased uptake of radioactive calcium produced by K‐252a is mediated by a mechanism very similar to that serving the increased calcium uptake produced by nerve growth factor. © 1995 Wiley‐Liss, Inc. This article is a US Government work and, as such, is in the public domain in the United States of America