Cellular mechanisms of potassium homeostasis in the mammalian nervous system

Double-barrelled ion-sensitive microelectrodes were used to measure
changes in the intracellular activities of K+, Na+, and Cl- (aKi,
aNai, aCli) in neurones of rat sympathetic ganglia and in glial
cells of slices from guinea-pig olfactory cortex. In sympathetic
neurones, carbachol and gamma-aminobutyric acid (GABA) produced a
reversible decrease of aKi. The decrease of aKi during carbachol
was accompanied by a rise of aNai, whereas in the presence of GABA
decreases of aKi and aCli were seen. The reuptake of K+ released
during the action of carbachol was completely blocked by ouabain,
whereas furosemide inhibited the aKi recovery after the action of
GABA. In glial cells, in contrast to the observations in the
sympathetic neurones, aKi and aCli increased, whereas aNai
decreased when neuronal activity was enhanced by repetitive
stimulation of the lateral olfactory tract. It was found that
barium ions and ouabain strongly reduced the activity-related rise
of intraglial aKi in slices of guinea-pig olfactory cortex. These
data show that mammalian neurones as well as glial cells possess
several K+ uptake mechanisms that contribute to potassium
homeostasis. Ouabain, furosemide, and Ba2+ are useful
pharmacological tools to separate these mechanisms.