Abstract
The effects of AlCl
3 on the production of
14CO
2 from [U-
14C] glucose and high affinity choline transport in rat brain synaptosomes, and on carbachol-stimulated hydrolysis of phosphoinositides in cortical slices were studied. In buffer containing either high K
+ (50 mM) or low K
+ (4.9 mM), 1 mM AlCl
3 significantly depressed the synaptosomal production of
14CO
2 from [U-
14C]-glucose to 54% and 44% of control rates, respectively. At a concentration of 0.1 mM, AlCl
3 depressed the evolution of
14CO
2 from [U-
14C]glucose from synaptosomes incubated in the high K
+ buffer, but did not significantly change
14CO
2 production from synaptosomes in the low K
+ buffer. Aluminum chloride also inhibited high affinity choline transport in synaptosomes prepared from rat cortex and from hippocampus with an IC
50 of approximately 0.5 mM. In brain slices the carbachol-stimulated hydrolysis of phosphoinositides was inhibited by AlCl
3 in a dose-dependent manner. One millimolar, 0.5 mM and 0.1 mM AlCl
3 inhibited the carbachol-stimulated release of inositol phosphates by 75%, 44% and 33%, respectively. These same concentrations of AlCl
3 inhibited the incorporation of [
3H] inositol into phospholipids. This inhibitory effect was not dose-dependent as all 3 concentrations of AlCl
3 inhibited phospholipid labelling to the same extent (27–37%). These results are discussed in relation to the in vivo neurotoxicity of aluminum.
