The whole-cell patch-clamp technique was applied to rat choroid plexus epithelial cells. The resting membrane potential was -53 mV. The whole-cell conductance was mainly K+ selective, and the K+ current observed appeared to contain two distinct components. Depolarizing voltage pulses (more positive than 0 mV) evoked time-dependent outward currents which resembled delayed-rectifying K+ currents in other tissues. The current exhibited time-dependent activation and, at potentials more positive than 40 mV, slower time-dependent inactivation. The reversal potential measured by tail current analysis showed a shift of 43 mV for a tenfold increase in extracellular K+ concentration ([K+]o). The current was reduced by extracellular 5 mM Ba2+, 5 mM tetraethylammonium (TEA+), 5 mM Cs+ and 1 mM 4-aminopyridine (4-AP). In contrast, hyperpolarizing voltage pulses evoked time-independent, inward-rectifying currents. The reversal potential measured by voltage-ramp commands showed a shift of 42 mV for a tenfold increase in [K+]o. The chord conductance did not appear to increase with increasing [K+]o. The current was reduced by extracellular 5 mM Ba2+ and 0.5 mM Cs+, but not by 5 mM TEA+ or 1 mM 4-AP. These data suggest that two populations of K+ channel contribute to the conductance of choroid plexus epithelial cells.

We herein report two cases of autoimmune gastritis without complete atrophy of the corpus. Both were positive for anti-parietal cell antibodies. Endoscopic examinations indicated that atrophic changes were predominant in the lesser curvature of the corpus in both cases. In one, the greater curvature was covered with pseudopolyp-like nodules, whereas the greater curvature of the other showed multiple similar nodules and mildly atrophic mucosa. Histopathological examinations of these nodules showed focal and patchy atrophy and preserved fundic glands with parietal cell pseudohypertrophy. Follow-up endoscopy and a repeated biopsy demonstrated the development of gastric atrophy on the greater curvature in both cases.

We have identified a whole-cell Cl- current activated by hyposmotic stress in rat lacrimal acinar cells using the patch-clamp technique. Superfusion of isolated single cells with hyposmotic solution (80% of control osmolarity) caused a gradual increase of the current, which was reversed on return to the control solution. The current-voltage relationship showed outward rectification, and the current showed time and voltage dependence: slowly activated by depolarizing voltages and rapidly inactivated by hyperpolarizing voltages. The increase in current was not observed when intracellular Ca2+ was chelated with EGTA. It was also inhibited by the absence of extracellular Ca2+, or the presence of gadolinium ions (20 microM Gd3+). We conclude that in rat lacrimal acinar cells hyposmotic stress activates Ca(2+)-dependent Cl- channels as a result of Ca2+ influx through a Gd(3+)-sensitive pathway. The Cl- channels involved appear to be indistinguishable from those activated by muscarinic stimulation. The inhibitory effect of Gd3+ suggests that stretch-activated nonselective cation channels may be responsible for the Ca2+ influx.