ArticleAntimicrobial agents and chemotherapy2008
Mefloquine-induced disruption of calcium homeostasis in mammalian cells is similar to that induced by ionomycin.
Article in Antimicrobial agents and chemotherapy, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 49 citations in OpenAlex.
- Article
- Broadband Electrical Spectroscopy to Distinguish Single-Cell CaSensors (Basel, Switzerland) · 2023Article
- Article
- Mefloquine induces ER stress and apoptosis in BRAFi-resistant A375-BRAFMolecular carcinogenesis · 2022Article
- Differential Stabilities of Mefloquine-Bound Human andACS omega · 2021Article
- Lead Optimization of Second-Generation Acridones as Broad-Spectrum Antimalarials.Journal of medicinal chemistry · 2020Article
- Effects of Constitutive and Acute Connexin 36 Deficiency on Brain-Wide Susceptibility to PTZ-Induced Neuronal Hyperactivity.Frontiers in molecular neuroscience · 2020Article
- INF2-mediated actin polymerization at the ER stimulates mitochondrial calcium uptake, inner membrane constriction, and division.The Journal of cell biology · 2018Article
- Pore-forming toxin-mediated ion dysregulation leads to death receptor-independent necroptosis of lung epithelial cells during bacterial pneumonia.Cell death and differentiation · 2017Article
- Neuronal pannexin-1 channels are not molecular routes of water influx during spreading depolarization-induced dendritic beading.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017Article
- Mefloquine in the nucleus accumbens promotes social avoidance and anxiety-like behavior in mice.Neuropharmacology · 2016Article
- Pore-Forming Toxins Induce Macrophage Necroptosis during Acute Bacterial Pneumonia.PLoS pathogens · 2015Article
- Effect of M-phase kinase phosphorylations on type 1 inositol 1,4,5-trisphosphate receptor-mediated Ca2+ responses in mouse eggs.Cell calcium · 2015Article
- A small-fish model for behavioral-toxicological screening of new antimalarial drugs: a comparison between erythro- and threo-mefloquine.BMC research notes · 2015Article
- The use of a prodrug approach to minimize potential CNS exposure of next generation quinoline methanols while maintaining efficacy in in vivo animal models.European journal of drug metabolism and pharmacokinetics · 2014Article
- Idiosyncratic quinoline central nervous system toxicity: Historical insights into the chronic neurological sequelae of mefloquine.International journal for parasitology. Drugs and drug resistance · 2014Article
- Mefloquine and psychotomimetics share neurotransmitter receptor and transporter interactions in vitro.Psychopharmacology · 2014Article
- Ketotifen is an antimalarial prodrug of norketotifen with blood schizonticidal and liver-stage efficacy.European journal of drug metabolism and pharmacokinetics · 2012Article
- The role of connexin-36 gap junctions in alcohol intoxication and consumption.Synapse (New York, N.Y.) · 2011Article
- Mefloquine effects on ventral tegmental area dopamine and GABA neuron inhibition: a physiologic role for connexin-36 GAP junctions.Synapse (New York, N.Y.) · 2011Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In previous studies, we have shown that mefloquine disrupts calcium homeostasis in neurons by depletion of endoplasmic reticulum (ER) stores, followed by an influx of external calcium across the plasma membrane. In this study, we explore two hypotheses concerning the mechanism(s) of action of mefloquine. First, we investigated the possibility that mefloquine activates non-N-methyl-d-aspartic acid receptors and the inositol phosphate 3 (IP3) signaling cascade leading to ER calcium release. Second, we compared the disruptive effects of mefloquine on calcium homeostasis to those of ionomycin in neuronal and nonneuronal cells. Ionomycin is known to discharge the ER calcium store (through an undefined mechanism), which induces capacitative calcium entry (CCE). In radioligand binding assays, mefloquine showed no affinity for the known binding sites of several glutamate receptor subtypes. The pattern of neuroprotection induced by a panel of glutamate receptor antagonists was dissimilar to that of mefloquine. Both mefloquine and ionomycin exhibited dose-related and qualitatively similar disruptions of calcium homeostasis in both neurons and macrophages. The influx of external calcium was blocked by the inhibitors of CCE in a dose-related fashion. Both mefloquine and ionomycin upregulated the IP3 pathway in a manner that we interpret to be secondary to CCE. Collectively, these data suggest that mefloquine does not activate glutamate receptors and that it disrupts calcium homeostasis in mammalian cells in a manner similar to that of ionomycin.
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