Membrane conductances during hypoosmotic swelling were characterized i
n rat astrocytes in primary tissue culture. Using whole cell patch cla
mp techniques, mean +/- SEM cell conductance in isoosmotic phosphate-b
uffered saline (PBS) was 55.6 +/- 5.8 pS/pF. Cell conductance (mean +/
- SEM) increased from this initial value to 187 +/- 46%, 561 +/- 188%,
and 1216 +/- 376% within 9 min of exposure to 220 mOsm, 190 mOsm, and
145 mOsm PBS, respectively. With each of these hypoosmotic exposures,
no change occurred in membrane capacitance. When CsCl replaced KCl in
the microelectrode solution, a similar conductance increase was obtai
ned at each osmolality. However, when gluconate salts were used in pla
ce of chloride salts in the electrode solution, no significant conduct
ance increase was observed with 190 mOsm PBS. With a KCl microelectrod
e solution, all conductance increase which occurred in 190 mOsm PBS wa
s inhibited by 200 mu M niflumic acid, but not by 5 mM BaCl2. Both nif
lumic acid and BaCl2 inhibited 60-80% of the conductance increase of c
ells in 145 mOsm PBS. Using a microelectrode solution containing tauri
ne as the major anion, membrane conductance increased 5-fold when cell
s were placed in 250 mOsm medium. This conductance increase was comple
tely inhibited by 200 mu M niflumic acid. Thus, independent chloride a
nd potassium conductances are activated by hypoosmotic swelling of cul
tured astrocytes while plasma membrane area is unaltered. The chloride
conductance pathway is activated at a significantly lower degree of h
ypoosmotic exposure than that which activates the potassium pathway an
d may be permeable to anionic taurine. These conductance pathways may
mediate diffusive loss of potassium, chloride, and taurine from these
cells during volume regulation following hypoosmotic swelling. (C) 199
7 Wiley-Liss, Inc.