Blockade of MTX-induced Ca2+ influx in rat glioma C6 cells by alkylamines

Keiichi Konoki, Masaki Hashimoto, Michio Murata, Kazuo Tachibana, Takeshi Yasumoto

Research output: Contribution to journalArticlepeer-review

4 Citations (Scopus)

Abstract

A series of alkylamines, namely, mono-, di-, and tri- hexylamine and tetra-hexyl-ammonium iodide, were tested for inhibition against Ca2+ influx by maitotoxin (MTX) in rat glioma C6 cells. The Ca2+ entry was monitored by 45Ca2+ influx and a Ca2+-sensitive fluorescent dye (fura- 2) assays. While hexylamine showed no significant inhibition, the other amines exhibited the potent inhibition upon 45Ca2+ influx assays along the increasing number of alkylation; dihexylamine with IC50 of ca. 50 μM, trihexylamine with ca. 20 μM, and tetrahexylammonium iodide with ca. 5 μM. C6 cells reportedly lack ion channels other than two types of K+ channels (delayed rectifier and Ca2+-activated channels), both of which are blocked by charybdotoxin. The toxin did not affect the MTX action, hence suggesting that the inhibition by the amines was not via K+ channels. Implication of membrane potential was also ruled out by experiments using a voltage- sensitive fluorescent dye, DiSC2(5), where these amines did not alter membrane potential in the presence of MTX. One of the possible explanations is that MTX interacts with a non-voltage-gated and usually inactive channel presumably belonging to the ion channel superfamily, through which the alkylamines block ion entry by the mechanism similar to that proposed for K+ channels.

Original languageEnglish
Pages (from-to)209-218
Number of pages10
JournalJournal of Natural Toxins
Volume5
Issue number2
Publication statusPublished - 1996 Jun 1
Externally publishedYes

ASJC Scopus subject areas

  • Environmental Science(all)
  • Toxicology

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