Effects of the Combined Treatment of Rats with Fluphenazine and Choline or Lecithin on the Striatal Cholinergic and Dopaminergic System

Abstract

It has been reported that the acute administration of choline (Ch) or its dietary precursor, lecithin (phosphatidylcholine; PCh) results in an increase in the steady-state concentration of acetylcholine (4, 11–13, 17). This increase was interpreted to be due to an enhanced ACh synthesis. Many clinical experiments have since been performed using Ch or PCh loading, based on the hypothesis that these agents would increase ACh levels, leading to an enhanced ACh release (for review see Bartus et al.; 2). In recent years, however, a number of groups have not been able to confirm the original finding of an increase in ACh levels in the brain or brain regions in rats or mice, after Ch or PCh administration (3, 7, 14, 18–23). Furthermore, no change in the synthesis rate of ACh has been observed after Ch loading (3, 6). Nevertheless, several reports have demonstrated that exogenous Ch or PCh could increase ACh content under conditions of increased cholinergic activity. In these investigations an attempt was made to increase activity by treatment of the animals with drugs like atropine, fluphenazine and pentylenetetrazol. It was observed that the decrease in ACh levels produced by these drugs in one or more regions of the brain could be attenuated by pretreatment of the animals with Ch or PCh (14, 19, 21–23, but see also 20 which failed to confirm these results).