Abstract
ACETYLCHOLINE (ACh) synthesis is coupled, in some unknown manner, to ACh release caused by neuronal impulse flow1–4. Accordingly, several models have been proposed regarding the regulation of ACh synthesis. These include feedback competitive inhibition of choline acetyl-transferase by ACh5,6, and mass action regulation of choline acetyltransferase7. More recently, high affinity choline uptake, which is very localised to cholinergic nerve terminals8, has been proposed as a regulatory step in ACh synthesis9–12. If high affinity choline uptake were coupled to ACh synthesis and release, then one would expect changes in the high affinity choline uptake system after alterations in synthesis and release. We have found changes in the high affinity choline uptake system in hippocampal synaptosomes after treatments which alter neuronal impulse flow to cholinergic nerve terminals.
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