We examined the effects of small unilamellar vesicles composed of dipalmitoylphosphatidylcholine on rat cerebral cortical 3Hacetylcholine release. Synaptosomes from this region were loaded with the labeled transmitter, and then incubated with the lipid (0–6 mg/ml) for specified intervals before adding various secretagogues. Liposomes (0.4 mg/ml–6 mg/ml) inhibited the calcium-dependent release of 3Hacetylcholine induced by 50 mM K+, A23187 (1–5 μg/ml) or 500 μM ouabain; the calcium-independent release induced by ouabain was not affected by the highest liposome concentration studied (6 mg/ml). 3HAcetylcholine levels were also reduced by the liposomes, but higher concentrations were necessary to do so than to reduce K+-induced release. These reductions occurred in the S3(cytosol) but not P3(microsomal) subcellular fraction of the nerve terminals. The 50 mM K+-induced induced release of 3Hnorepinephrine and 3Hdopamine from cerebral cortical and striatal synaptosomes, respectively, were not affected by 6 mg/ml lipid. Together, these results suggest that the dipalmitoylphosphatidylcholine liposomes may modulate cholinergic transmission presynaptically at the level of the calcium-dependent transmitter-release
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