Activation of chloride currents in choroid plexus by GTP-gamma-S and cyclic-AMP.
The regulation of a Cl- conductance in the choroid plexus by G proteins was investigated using whole-cell patch clamp methods. A transient Cl- current was evoked when GTP-gamma-S (0.1 mM) was included in the electrode solution. The GTP-gamma-S-evoked current was only observed when 2 mM ATP was present in the electrode solution, and was inhibited in the presence of 2 mM GDP-beta-S. The activated current was shown to be Cl(-)-selective in ion replacement studies, and exhibited inward-rectification. The current was not inhibited when intracellular Ca2+ was strongly buffered with either EGTA or BAPTA, suggesting that the current was not activated by a change in intracellular Ca2+. The effects of GTP-gamma-S were mimicked, however, when cyclic AMP or the catalytic-subunit of protein kinase A were included in the electrode solution. These data suggest that G proteins activate Cl- channels via a cAMP-dependent pathway in rat choroid plexus.
Kotera
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T
Cell Physiology Group, School of Biological Sciences, University of Manchester, UK.
Brown
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PD
D000255:Adenosine Triphosphate / Q000494:pharmacology; D000818:Animals; D018118:Chloride Channels / Q000502:physiology*; D002831:Choroid Plexus / Q000502:physiology*; D000242:Cyclic AMP / Q000494:pharmacology*; D004848:Epithelium; D018698:Glutamic Acid / Q000494:pharmacology; D006160:Guanosine Triphosphate / Q000494:pharmacology*; D018408:Patch-Clamp Techniques; D051381:Rats
D018118:Chloride Channels; D018698:Glutamic Acid; D006160:Guanosine Triphosphate; D000255:Adenosine Triphosphate; D000242:Cyclic AMP