Acetylcholine release in the cat caudate nucleus measured with the choline oxidase method.

A chemiluminescent assay for the estimation of acetylcholine (ACh) was used to measure ACh release in caudate nuclei (CN) of halothane-anaesthetized cats implanted with push-pull cannulae. The validity of the entire experimental approach used was shown by the fact that ACh release was calcium-dependent and was increased by depolarizing agents (potassium ions, veratridine) as well as by atropine. The effects of GABA (10(-5) M, 30 min) unilateral application into the ventralis medialis and ventralis lateralis thalamic nuclei on ACh release in both CN were then examined.

Inhibition by trimethyl-tin, probenecid and phenylglyoxal of depolarization-induced acetylcholine release in Torpedo synaptosomes.

The effects of trimethyl-tin (anion-hydroxyde ionophore, inhibiting oxydative phosphorylation and H(+)-ATPase) probenecid (inhibitor of anion transport in neural cells) and phenylglyoxal (arginine-specific reagent, inhibiting chloride exchanges in erythrocytes) were examined in Torpedo synaptosomes prepared from electric organ. All drugs significantly reduced the stimulated release of acetylcholine triggered by depolarization of nerve endings with high-K(+) and/or gramicidin D. In contrast, trimethyl-tin, probenecid and phenylglyoxal did not affect the ionophore A23187-induced release of acetylcholine from the synaptosomes.

Acetylcholine incorporation by cholinergic synaptic vesicles from Torpedo marmorata.

The ability of cholinergic vesicles to incorporate acetylcholine (ACh) was studied using highly purified synaptic vesicles from Torpedo electric organ. Depleted vesicles were capable of rapidly taking up exogenous ACh. Evidence that this represented true incorporation was that labelled ACh comigrated with vesicular ATP on gel filtration and that vesicle-associated ACh was protected against enzymatic hydrolysis and was releasable under hypoosmotic conditions.