TY - JOUR
T1 - Potassium and taurine release are highly correlated with regulatory volume decrease in neonatal primary rat astrocyte cultures
AU - Vitarella, Domenico
AU - DiRisio, Darryl J.
AU - Kimelberg, Harold K.
AU - Aschner, Michael
N1 - Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.
PY - 1994/9
Y1 - 1994/9
N2 - Neonatal rat primary astrocyte cultures were swollen by exposure to hypotonic buffer. Using an electrical impedance method for determination of cell volume coupled with on-line measurements of efflux of radioactive ions or amino acids, we have investigated the role of K+ (using 86Rb), taurine, and D-aspartate (an analogue of glutamate) in regulatory volume decrease (RVD). Addition of 1 mM quinine, 10 μM nimodipine, 100 μM BAPTA-AM, 10 μM trifluoperazine, or a calcium-free buffer significantly (p < 0.0001) inhibited RVD. This was accompanied by inhibition of 86Rb release but an increase in D-[3H]aspartate release, which was proportional to the degree to which RVD was inhibited. These results support a regulatory role for calcium in RVD and show that inhibition of calcium entry from the extracellular fluid, intracellular calcium sequestration, inhibition of calcium-activated K+ channels, and inhibition of calmodulin all inhibit RVD. Because D- [3H]aspartate efflux profiles increase as RVD is inhibited, it is unlikely that D-aspartate release is a main determinant of RVD. In contrast, [3H]taurine release was increased by 1 mM quinine and inhibited by 10 μM trifluoperazine. The net release of K+ and taurine is highly correlated with the degree of RVD, implicating a regulatory role for both K+ and taurine release in RVD.
AB - Neonatal rat primary astrocyte cultures were swollen by exposure to hypotonic buffer. Using an electrical impedance method for determination of cell volume coupled with on-line measurements of efflux of radioactive ions or amino acids, we have investigated the role of K+ (using 86Rb), taurine, and D-aspartate (an analogue of glutamate) in regulatory volume decrease (RVD). Addition of 1 mM quinine, 10 μM nimodipine, 100 μM BAPTA-AM, 10 μM trifluoperazine, or a calcium-free buffer significantly (p < 0.0001) inhibited RVD. This was accompanied by inhibition of 86Rb release but an increase in D-[3H]aspartate release, which was proportional to the degree to which RVD was inhibited. These results support a regulatory role for calcium in RVD and show that inhibition of calcium entry from the extracellular fluid, intracellular calcium sequestration, inhibition of calcium-activated K+ channels, and inhibition of calmodulin all inhibit RVD. Because D- [3H]aspartate efflux profiles increase as RVD is inhibited, it is unlikely that D-aspartate release is a main determinant of RVD. In contrast, [3H]taurine release was increased by 1 mM quinine and inhibited by 10 μM trifluoperazine. The net release of K+ and taurine is highly correlated with the degree of RVD, implicating a regulatory role for both K+ and taurine release in RVD.
KW - Aspartate
KW - Astrocytes
KW - Calcium
KW - Taurine
KW - Volume regulation
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U2 - 10.1046/j.1471-4159.1994.63031143.x
DO - 10.1046/j.1471-4159.1994.63031143.x
M3 - Article
C2 - 8051556
AN - SCOPUS:0028074718
SN - 0022-3042
VL - 63
SP - 1143
EP - 1149
JO - Journal of Neurochemistry
JF - Journal of Neurochemistry
IS - 3
ER -