Functional Exploration Of T-Type Calcium Channels (Cav3.2 And Cav3.3) And Their Sensitivity To Zinc

Overview

Journal Open Microbiol J

Publisher Bentham Open

Specialty Microbiology

Date 2018 Sep 11

PMID 30197701

Citations 1

Authors

Tahar Hazzaz Abouamal

Zineb Choukairi

Fechtali Taoufiq

Affiliations

Soon will be listed here.

Abstract

Introduction: T-type Ca channels (TTCC) are low Voltage-gated calcium channels, expressed in various tissues such as the brain and heart, and contribute to a variety of physiological functions including neuronal excitability, hormone secretion, muscle contraction, and pacemaker activity. At high concentrations, Zinc (Zn) is naturally attached to cell membranes and is therefore considered a reversible inhibitor of calcium. Zinc is also involved in the kinetics of sodium and potassium currents. Zinc is essential for many functions. A low zinc tenor is associated with emotional instability, digestive disorders, slow-growing and alteration of protein synthesis.

Material And Methods: For the Cell Culture we used HEK-293/tsA-201, and for transfection, the pCDNA3 plasmid constructs encoding human CaV3.2, and CaV3.3 subunits. Electrophysiological experiments were performed using the whole cell configuration of the patch-clamp technique. T-type currents were recorded using a test pulse from a holding potential at (-100mV) to (-30 mV), data Acquisition and Analysis for Current-voltage relationships (I-V curves) were recorded for the two cloned T-type Ca channels (Cav3.2, Cav3.3).

Results: Our studies describe the behavior of these channels Cav3.2 and Cav3.3 and also their current sensitivity to Zinc (Zn) in transfected HEK-293/tsA-201cells. Our results show that Zn applies a modulatory effect on T-type calcium channels. We observe that Zn differentially modulates the CaV3.2 and CaV3.3 channels. Zn preferably inhibits Cav3.2.

Conclusion: We have demonstrated that Zn differentially modulates two CaV3 channels (Cav3.2 and Cav3.3): It is a preferential blocker of CaV3.2 channels and it alters the gating behaviour of CaV3.3 channels.

Citing Articles

Hydrogen Sulfide-Evoked Intracellular Ca Signals in Primary Cultures of Metastatic Colorectal Cancer Cells.

Faris P, Ferulli F, Vismara M, Tanzi M, Negri S, Rumolo A Cancers (Basel). 2020; 12(11).

PMID: 33187307 PMC: 7696676. DOI: 10.3390/cancers12113338.

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