Gap junctions between glial cells allow intercellular exchange of ions
and small molecules. We have investigated the influence of gap juncti
on coupling on regulation of intracellular Na+ concentration ([Na+](i)
) in cultured rat hippocampal astrocytes, using fluorescence ratio ima
ging with the Na+ indicator dye SBFI (sodium-binding benzofuran isopht
halate). The [Na+](i) in neighboring astrocytes was very similar (12.0
+/- 3.3 mM), and did not fluctuate under resting conditions. During u
ncoupling of gap junctions with octanol (0.5 mM), baseline [Na+](i) wa
s unaltered in 24%, increased in 54%, and decreased in 22% of cells. Q
ualitatively similar results were obtained with two other uncoupling a
gents, heptanol and alpha-glycyrrhetinic acid (AGA). Octanol did not a
lter the recovery from intracellular Na+ load induced by removal of ex
tracellular K+, indicating that octanol's effects on baseline [Na+](i)
were not due to inhibition of Na+, K+-ATPase activity. Under control
conditions, increasing [K+](o) from 3 to 8 mM caused similar decreases
in [Na+](i) in groups of astrocytes, presumably by stimulating Na+, K
+-ATPase. During octanol application, [K+](o)-induced [Na+](i) decreas
es were amplified in cells with increased baseline [Na+](i), and reduc
ed in cells with decreased baseline [Na+](i). This suggests that basel
ine [Na+](i) in astrocytes ''sets'' the responsiveness of Na+, K+-ATPa
se to increases in [K+](o). Our results indicate that individual hippo
campal astrocytes in culture rapidly develop different levels of basel
ine [Na+](i) when they are isolated from one another by uncoupling age
nts. In astrocytes, therefore, an apparent function of coupling is the
intercellular exchange of Na+ ions to equalize baseline [Na+](i), whi
ch serves to coordinate physiological responses that depend on the int
racellular concentration of this ion. (C) 1997 Wiley-Liss, Inc.