ArticleInvertebrate neuroscience : IN1998
Trifluoperazine enhancement of Ca2+-dependent inactivation of L-type Ca2+ currents in Helix aspersa neurons.
Article in Invertebrate neuroscience : IN, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 3 citations in OpenAlex.
- Sigma-1 Receptor Ligands Chlorpromazine and Trifluoperazine Attenuate CaCell and tissue biology · 2022Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The effects of trifluoperazine hydrochloride (TFP), a calmodulin antagonist, on L-type Ca2+ currents (L-type ICa2+) and their Ca(2+)-dependent inactivation, were studied in identified Helix aspersa neurons, using two microelectrode voltage clamp. Changes in [Ca2+]i were measured in unclamped fura-2 loaded neurons. Bath applied TFP produced a reversible and dose-dependent reduction in amplitude of L-type ICa2+ (IC50 = 28 microM). Using a double-pulse protocol, we found that TFP enhances the efficacy of Ca(2+)-dependent inactivation of L-type ICa2+. Trifluoperazine sulfoxide (50 microM), a TFP derivative with low calmodulin-antagonist activity, did not have any effects on either amplitude or inactivation of L-type ICa2+. TFP (20 microM) increased basal [Ca2+]i from 147 +/- 37 nM to 650 +/- 40 nM (N = 7). The increase in [Ca2+]i was prevented by removal of external Ca2+ and curtailed by depletion of caffeine-sensitive intracellular Ca2+ stores. Since TFP may also block protein kinase C (PKC), we tested the effect of a PKC activator (12-C-tetradecanoyl-phorbol-13-acetate) on L-type Ca2+ currents. This compound produced an increase in L-type ICa2+ without enhancing Ca(2+)-dependent inactivation. The results show that 1) TFP reduces L-type ICa2+ while enhancing the efficacy of Ca(2+)-dependent inactivation. 2) TFP produces an increase in basal [Ca2+]i which may contribute to the enhancement of Ca(2+)-dependent inactivation. 3) PKC up-regulates L-type ICa2+ without altering the efficacy of Ca(2+)-dependent inactivation. 4) The TFP effects cannot be attributed to its action as PKC blocker.
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Registered trials
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