CA2-86 EFFLUX ACTIVATED BY HYPOSMOLARITY IN CEREBELLAR GRANULE NEURONS( CHANGES AND RB)

Hyposmotic swelling increased Rb-86 release in cultured cerebellar gra nule neurons (1 day in vitro [DIV]) with a magnitude related to the ch ange in osmolarity. Rb-86 release was partially blocked by quinidine, Ba2+, and Cs+ but not by TEA, 4-AP, or Gd3+, Rb-86 efflux decreased in CI--depleted cells or cells treated with DDF or DIDS, suggesting are interconnection between Cl- sand K+ fluxes, Swelling induced a substan tial increase in [Ca2+](i) to which both external and internal sources contribute, However, Rb-86 efflux was independent of [Ca2+](i), unaff ected by depleting the endoplasmic reticulum (ER) by ionomycin or thap sigargin and insensitive to charybdotoxin, iberiotoxin, and apamin. Sw elling-activated Rb-86 efflux in differentiated granule neurons after 8 DIV, which express Ca2+-sensitive K+ channels, was not different fro m that in 1 DIV neurons, nor in time course, net release, Ca2+-depende nce, or pharmacological sensitivity. We conclude that the swelling-act ivated K+ efflux in cerebellar granule neurons is not mediated by Ca2-sensitive large conductance K+ channels (BK) as in many cell types bu t resembles that in lymphocytes where it is possibly carried by voltag e-gated K+ channels. (C) 1998 Wiley-Liss,Inc.