Abstract
At peripheral cholinergic nerve terminals, lanthanum (La 3+) increases acetylcholine (ACh) release and supports transmitter release induced by α-latrotoxin (α-LTx). The present experiments investigate these interactions at central cholinergic nerve terminals by measuring the effects of La 3+ and gadolinium (Gd 3+), another element of the lathanide (Ln 3+) series, on ACh release and free intracellular calcium concentrations ([Ca 2+] i) in rat cortical synaptosomal preparations. Ln 3+ had no measurable effect on basal synaptosomal ACh release, ACh contents or [Ca 2+] i. Release of ACh induced by α-LTx was inhibited by the presence of Ln 3+, as were ACh release responses to elevated K +. The rise in [Ca 2+] i induced by α-LTx was inhibited by Ln 3+ at concentrations similar to those that inhibited ACh release. Addition of Ln 3+ subsequent to an α-LTx-evoked increase in [Ca 2+] i resulted in an immediate (within 4 s) cessation of calcium entry. Gd 3+ binding studies using the radioisotope 153Gd 3+ revealed that Gd 3+ bound extremely rapidly to synaptosomes and that under the experimental conditions used to measure either α-LTx- or K +-induced ACh release, little or no free Gd 3+ was likely to exist in the medium. We conclude that at central cholinergic neurons 1-Ln 3+ do not affect basal ACh release and 2-Ln 3+ are effective inhibitors for α-LTx-induced ACh release and changes in [Ca 2+] i.
Published Version
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