Chloride efflux from isolated choroid plexus.
Chloride efflux was analyzed in adult rat lateral ventricle choroid plexus (LVCP) incubated in artificial CSF (aCSF) at 37 degrees C. Following steady-state loading of 36Cl in LVCP, the tracer release from plexus to aCSF was quantified by the efflux coefficient (k, s-1), equal to ln 2/t/2. Cl efflux could be described by a 2-component model, with a t/2 for the 'fast' component matching well that for [3H]sucrose (extracellular marker) and a slower, drug-inhibitable component of 36Cl release thought to reflect cellular washout. The cellular Cl efflux was more than twice as fast as 37 degrees C than at 15 degrees C. There was progressively more rapid efflux (k) of 36Cl from cells as the aCSF was altered over a range of several pH values from 6.7 (k = 0.026 s-1) to 8.2 (0.070 s-1). CSF medium anion replacement (isethionate and HEPES for Cl and HCO3, respectively) reduced the k for 36Cl by 57%. Acetazolamide (0.1 mM) and other Cl transport inhibitors (disulfonic stilbenes and loop diuretic) reduced Cl efflux by 35-55%. Acetazolamide inhibited Cl release from LVCP into aCSF whether the latter contained Cl and HCO3, or not. Overall, the findings suggest that Cl extrusion from choroid plexus is by way of an anion exchanger and via channels.
Smith
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Laboratory of Neurosciences, National Institute on Aging, NIH, Bethesda, MD 20892.
Johanson
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CE
D000086:Acetazolamide / Q000494:pharmacology; D000136:Acid-Base Equilibrium / Q000502:physiology; D000818:Animals; D002712:Chlorides / Q000134:cerebrospinal fluid / Q000378:metabolism*; D002831:Choroid Plexus / Q000378:metabolism*; D003080:Cold Temperature; D004232:Diuretics / Q000494:pharmacology; D006531:HEPES; D006863:Hydrogen-Ion Concentration; D066298:In Vitro Techniques; D007513:Isethionic Acid; D051381:Rats; D011919:Rats, Inbred Strains
D002712:Chlorides; D004232:Diuretics; D007513:Isethionic Acid; D000086:Acetazolamide; D006531:HEPES