The uptake and efflux of Cl-36 in the lateral ventricle choroid plexus
of 1-7-week-old rats were measured to determine if Cl transport chang
ed with age and if such transport responded to inhibitors of CSF secre
tion and ion transport. The steady-state (30 min) Cl uptakes were 148/-9.4 nmol.mg-1 dry weight at 1 week and 139+/-7.0 nmol.mg-1 dry weigh
t at 7 weeks, (P > 0.05). The Cl-36 efflux was significantly slower in
1 and 2 week plexuses compared to more mature tissues (P < 0.01) with
k (rate coefficient) = 0.029+/-0.004 s-1, t1/2 = 24.1+/-3.3 s at 1 we
ek and k = 0.041+/-0.003 s-1, t1/2 = 17.4+/-1.3 s at 7 weeks. Cl-36 ef
flux at 1 week was unaffected by acetazolamide, bumetanide and DIDS (4
,4 diisothiocyanato-stilbene-2,2 disulphonic acid), however, all these
drugs substantially reduced efflux from 2, 3 and 7 week choroid plexu
ses. In contrast, the Cl conductance blocker, DPC (diphenylamine carbo
xylate) at 10(-4) M reduced Cl-36 efflux from both 1 and 7 week tissue
s by 43% and 39%, respectively. These findings suggest that some trans
port systems responsible for movement of Cl out of the epithelium are
either absent or less functional in the immature rat choroid plexus an
d may account for the relatively low level of CSF secretion in younger
animals. The unidirectional efflux of Cl-36, J, was calculated for 1
week and adult rats, as a function of the choroid plexus volume to sur
face area ratio (V/A). Efflux was close to 550 nmol.cm-2.s-1 at both a
ges indicating that enhanced Cl-36 efflux with age is mainly a functio
n of increasing epithelial cell surface area.