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Ca 2+ changes and 86 Rb efflux activated by hyposmolarity in cerebellar granule neurons
Author(s) -
MoralesMulia Sandra,
Ordaz Benito,
Quesada Octavio,
PasantesMorales Herminia
Publication year - 1998
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/(sici)1097-4547(19980901)53:5<626::aid-jnr12>3.0.co;2-z
Subject(s) - apamin , efflux , granule (geology) , charybdotoxin , ionomycin , chemistry , biophysics , microbiology and biotechnology , potassium channel , biology , biochemistry , in vitro , paleontology
Hyposmotic swelling increased 86 Rb release in cultured cerebellar granule neurons (1 day in vitro [DIV]) with a magnitude related to the change in osmolarity. 86 Rb release was partially blocked by quinidine, Ba 2+ , and Cs + but not by TEA, 4‐AP, or Gd 3+ . 86 Rb efflux decreased in Cl − ‐depleted cells or cells treated with DDF or DIDS, suggesting an interconnection between Cl − and K + fluxes. Swelling induced a substantial increase in [Ca 2+ ] i to which both external and internal sources contribute. However, 86 Rb efflux was independent of [Ca 2+ ] o , unaffected by depleting the endoplasmic reticulum (ER) by ionomycin or thapsigargin and insensitive to charybdotoxin, iberiotoxin, and apamin. Swelling‐activated 86 Rb efflux in differentiated granule neurons after 8 DIV, which express Ca 2+ ‐sensitive K + channels, was not different from that in 1 DIV neurons, nor in time course, net release, Ca 2+ ‐dependence, or pharmacological sensitivity. We conclude that the swelling‐activated K + efflux in cerebellar granule neurons is not mediated by Ca 2+ ‐sensitive large conductance K + channels (BK) as in many cell types but resembles that in lymphocytes where it is possibly carried by voltage‐gated K + channels. J. Neurosci. Res. 53:626–635, 1998. © 1998 Wiley‐Liss, Inc.