4-Аminopyridine sequesters intracellular Ca2+ which triggers exocytosis in excitable and non-excitable cells View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-12

AUTHORS

Ludmila A Kasatkina

ABSTRACT

4-aminopyridine is commonly used to stimulate neurotransmitter release resulting from sustained plasma membrane depolarization and Ca2+-influx from the extracellular space. This paper elucidated unconventional mechanism of 4-aminopyridine-stimulated glutamate release from neurons and non-neuronal cells which proceeds in the absence of external Ca2+. In brain nerve terminals, primary neurons and platelets 4-aminopyridine induced the exocytotic release of glutamate that was independent of external Ca2+ and was triggered by the sequestration of Ca2+ from intracellular stores. The initial level of 4-aminopyridine-stimulated glutamate release from neurons in the absence or presence of external Ca2+ was subequal and the difference was predominantly associated with subsequent tonic release of glutamate in Ca2+-supplemented medium. The increase in [Ca2+]i and the secretion of glutamate stimulated by 4-aminopyridine in Ca2+-free conditions have resulted from Ca2+ efflux from endoplasmic reticulum and were abolished by intracellular free Ca2+ chelator BAPTA. This suggests that Ca2+ sequestration plays a profound role in the 4-aminopyridine-mediated stimulation of excitable and non-excitable cells. 4-Aminopyridine combines the properties of depolarizing agent with the ability to sequester intracellular Ca2+. The study unmasks additional mechanism of action of 4-aminopyridine, an active substance of drugs for treatment of multiple sclerosis and conditions related to reduced Ca2+ efflux from intracellular stores. More... »

PAGES

34749

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/srep34749

DOI

http://dx.doi.org/10.1038/srep34749

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PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/27703262


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56 schema:description 4-aminopyridine is commonly used to stimulate neurotransmitter release resulting from sustained plasma membrane depolarization and Ca<sup>2+</sup>-influx from the extracellular space. This paper elucidated unconventional mechanism of 4-aminopyridine-stimulated glutamate release from neurons and non-neuronal cells which proceeds in the absence of external Ca<sup>2+</sup>. In brain nerve terminals, primary neurons and platelets 4-aminopyridine induced the exocytotic release of glutamate that was independent of external Ca<sup>2+</sup> and was triggered by the sequestration of Ca<sup>2+</sup> from intracellular stores. The initial level of 4-aminopyridine-stimulated glutamate release from neurons in the absence or presence of external Ca<sup>2+</sup> was subequal and the difference was predominantly associated with subsequent tonic release of glutamate in Ca<sup>2+</sup>-supplemented medium. The increase in [Ca<sup>2+</sup>]<sub>i</sub> and the secretion of glutamate stimulated by 4-aminopyridine in Ca<sup>2+</sup>-free conditions have resulted from Ca<sup>2+</sup> efflux from endoplasmic reticulum and were abolished by intracellular free Ca<sup>2+</sup> chelator BAPTA. This suggests that Ca<sup>2+</sup> sequestration plays a profound role in the 4-aminopyridine-mediated stimulation of excitable and non-excitable cells. 4-Aminopyridine combines the properties of depolarizing agent with the ability to sequester intracellular Ca<sup>2+</sup>. The study unmasks additional mechanism of action of 4-aminopyridine, an active substance of drugs for treatment of multiple sclerosis and conditions related to reduced Ca<sup>2+</sup> efflux from intracellular stores.
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