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 Cl-36 in LVCP, the tracer release from plexus to aCSF was quantified by the efflux coefficient (k, s-1), equal to ln 2/t1/2. Cl efflux could be described by a 2-component model, with a t1/2 for the 'fast' component matching well that for [H-3]sucrose (extracellular marker) and a slower, drug-inhibitable component of Cl-36 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 Cl-36 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 Cl-36 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.