Abstract
INTRODUCTION: T-type Ca(2+) 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(2+)) 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(2+) 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(2+)) in transfected HEK-293/tsA-201cells. Our results show that Zn(2+) applies a modulatory effect on T-type calcium channels. We observe that Zn(2+) differentially modulates the CaV3.2 and CaV3.3 channels. Zn(2+) preferably inhibits Cav3.2. CONCLUSION: We have demonstrated that Zn(2+) 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.