D. Gunzel et al., INTRACELLULAR ALKALINIZATION CAUSES MG2-SITES IN LEECH RETZIUS NEURONS( RELEASE FROM INTRACELLULAR BINDING), Pflugers Archiv, 435(1), 1997, pp. 65-73
Four-barrelled ion-sensitive microelectrodes were developed to enable
simultaneous measurement of intracellular free Mg2+ and Naf concentrat
ions ([Mg2+](i), [Na+](i)), intracellular pH and the membrane potentia
l. The electrodes were used to investigate pH-induced [Mg2+](i) change
s in Retzius neurones of the leech Hirudo medicinalis. The application
of propionate or CO2/HCO3--buffered bath solutions caused a transient
intracellular acidification, an initial [Mg2+](i) decrease and a cont
inuous [Na+](i) increase. In the presence of CO2/HCO3- this [Na+](i) i
ncrease was more pronounced and might be the reason for the slow incre
ase in [Mg2+](i) following the initial decrease. The withdrawal of pro
pionate or CO2/HCO3--buffered bath solutions caused a transient alkali
nization which was accompanied by a slight but significant [Mg2+](i) i
ncrease, even in the nominal absence of extracellular Mg2+, while [Na](i) returned to its original value. The alkalinization-induced [Mg2+]
(i) increase could be reduced to about 50% by the application of 1-10
mu M cyclosporin A, an inhibitor of the mitochondrial permeability tra
nsition pore (MTP). Phenylarsine oxide, an MTP activator, caused a [Mg
2+](i) increase with characteristics similar to those of the alkaliniz
ation-induced increase, which could not be attributed to any changes i
n [Na+](i) or pH(i). It is concluded that an intracellular alkalinizat
ion might induce the release of Mg2+ from intracellular stores.