The acute neurotoxicity of mefloquine may be mediated through a disruption of calcium homeostasis and ER function in vitro.

ABSTRACT:

Background

There is no established biochemical basis for the neurotoxicity of mefloquine. We investigated the possibility that the acute in vitro neurotoxicity of mefloquine might be mediated through a disruptive effect of the drug on endoplasmic reticulum (ER) calcium homeostasis.

Methods

Laser scanning confocal microscopy was employed to monitor real-time changes in basal intracellular calcium concentrations in embryonic rat neurons in response to mefloquine and thapsigargin (a known inhibitor of the ER calcium pump) in the presence and absence of external calcium. Changes in the transcriptional regulation of known ER stress response genes in neurons by mefloquine were investigated using Affymetrix arrays. The MTT assay was employed to measure the acute neurotoxicity of me

SUBMITTER: Dow GS 

PROVIDER: S-EPMC194860 | biostudies-literature | 2003 Jun

REPOSITORIES: biostudies-literature