Enhancement of 45Ca2+ influx and voltage-dependent Ca2+ channel activity by β-amyloid-(1-40) in rat cortical synaptosomes and cultured cortical neurons. Modulation by the proinflammatory cytokine interleukin-1β

Aoife MacManus, Martin Ramsden, Michael Murray, Zaineb Henderson, Hugh A. Pearson, Veronica A. Campbell

Research output: Contribution to journalArticlepeer-review

127 Citations (Scopus)

Abstract

β-Amyloid protein is thought to underlie the neurodegeneration associated with Alzheimer's disease by inducing Ca2+-dependent apoptosis. Elevated neuronal expression of the proinflammatory cytokine interleukin-1β is an additional feature of neurodegeneration, and in this study we demonstrate that interleukin-1β modulates the effects of β-amyloid on Ca2+ homeostasis in the rat cortex. β-Amyloid-(1-40) (1 μM) caused a significant increase in 45Ca2+ influx into rat cortical synaptosomes via activation of L- and N-type voltage-dependent Ca2+ channels and also increased the amplitude of N- and P-type Ca2+ channel currents recorded from cultured cortical neurons. In contrast, interleukin-1β (5 ng/ml) reduced the 45Ca2+ influx into cortical synaptosomes and inhibited Ca2+ channel activity in cultured cortical neurons. Furthermore, the stimulatory effects of β-amyloid protein on Ca2+ influx were blocked following exposure to interleukin-1β, suggesting that interleukin-1β may govern neuronal responses to β-amyloid by regulating Ca2+ homeostasis.

Original languageEnglish
Pages (from-to)4713-4718
Number of pages6
JournalJournal of Biological Chemistry
Volume275
Issue number7
DOIs
Publication statusPublished - 18 Feb 2000
Externally publishedYes

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