Helothermine, a lizard venom toxin, inhibits calcium current in cerebellar granules

1996 ◽  
Vol 110 (1) ◽  
Author(s):  
Mario Nobile ◽  
Francesca Noceti ◽  
Gianfranco Prestipino ◽  
LourivalD. Possani
2000 ◽  
Vol 5 (4) ◽  
pp. 245-245
Author(s):  
Qh Hogan ◽  
Jb McCallum ◽  
C Sarantopoulos ◽  
M Aason ◽  
M Mynlieff ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Iva Synková ◽  
Markéta Bébarová ◽  
Irena Andršová ◽  
Larisa Chmelikova ◽  
Olga Švecová ◽  
...  

AbstractThe variant c.926C > T (p.T309I) in KCNQ1 gene was identified in 10 putatively unrelated Czech families with long QT syndrome (LQTS). Mutation carriers (24 heterozygous individuals) were more symptomatic compared to their non-affected relatives (17 individuals). The carriers showed a mild LQTS phenotype including a longer QTc interval at rest (466 ± 24 ms vs. 418 ± 20 ms) and after exercise (508 ± 32 ms vs. 417 ± 24 ms), 4 syncopes and 2 aborted cardiac arrests. The same haplotype associated with the c.926C > T variant was identified in all probands. Using the whole cell patch clamp technique and confocal microscopy, a complete loss of channel function was revealed in the homozygous setting, caused by an impaired channel trafficking. Dominant negativity with preserved reactivity to β-adrenergic stimulation was apparent in the heterozygous setting. In simulations on a human ventricular cell model, the dysfunction resulted in delayed afterdepolarizations (DADs) and premature action potentials under β-adrenergic stimulation that could be prevented by a slight inhibition of calcium current. We conclude that the KCNQ1 variant c.926C > T is the first identified LQTS-related founder mutation in Central Europe. The dominant negative channel dysfunction may lead to DADs under β-adrenergic stimulation. Inhibition of calcium current could be possible therapeutic strategy in LQTS1 patients refractory to β-blocker therapy.


1998 ◽  
Vol 18 (1) ◽  
pp. 112-118 ◽  
Author(s):  
Malgorzata A. Wilk-Blaszczak ◽  
Bernd Stein ◽  
Shuichan Xu ◽  
Miguel S. Barbosa ◽  
Melanie H. Cobb ◽  
...  

2005 ◽  
Vol 90 (7) ◽  
pp. 4191-4197 ◽  
Author(s):  
Bo Liu ◽  
Stephen J. Hill ◽  
Raheela N. Khan

Abstract Context: Little is known about the crosstalk between the decidua and myometrium in relation to human labor. The hormone oxytocin (OT) is considered to be a key mediator of uterine contractility during parturition, exerting some of its effects through calcium channels. Objective: The objective was to characterize the effect of OT on the T-type calcium channel in human decidual stromal cells before and after the onset of labor. Design: The nystatin-perforated patch-clamp technique was used to record inward T-type calcium current (ICa(T)) from acutely dispersed decidual stromal cells obtained from women at either elective cesarean section [CS (nonlabor)] or after normal spontaneous vaginal delivery [SVD (labor)]. Setting: These studies took place at the University of Nottingham Medical School. Results: I Ca(T) of both SVD and CS cells were blocked by nickel (IC50 of 5.6 μm) and cobalt chloride (1 mm) but unaffected by nifedipine (10 μm). OT (1 nm to 3.5 μm) inhibited ICa(T) of SVD cells in a concentration-dependent manner, with a maximal inhibition of 79.0% compared with 26.2% in decidual cells of the CS group. OT-evoked reduction of ICa(T) was prevented by preincubation with the OT antagonist L371,257 in the SVD but not CS group. OT, in a concentration-dependent manner, displaced the steady-state inactivation curve for ICa(T) to the left in the SVD group with no significant effect on curves of the CS group. Conclusion: Inhibition of ICa(T) by OT in decidual cells obtained during labor may signify important functional remodeling of uterine signaling during this period.


1982 ◽  
Vol 244 (1) ◽  
pp. 135-144 ◽  
Author(s):  
Martin Galvan ◽  
Paul R. Adams

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