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- Nelson, M.T. et al. (2007) J. Neurosci. 27, 12577.
- Alomone Labs L-Ascorbic acid inhibits T-type voltage-gated Ca2+ currents expressed in Xenopus oocytes.A. Time course of CaV3.2/β3 (T-type) current inhibition by 5 µM of L-Ascorbic acid (#L-140). Currents were elicited by application of voltage ramps from a holding potential of -100 mV to 20 mV (100 msec) delivered every 10 seconds. B. Superimposed example traces of current responses before and during perfusion of 5 µM L-Ascorbic acid as indicated.
- Nilius, B. et al. (2006) Cell Calcium 40, 81.
- Perez-Reyes, E. and Lory, P. (2006) CNS Neurol. Disord. Drug Targets 5, 605.
- Talavera, K. and Nilius, B. (2006) Cell Calcium 40, 97.
- Nelson, M.T. et al. (2007) J. Neurosci. 27, 12577.
The T-type calcium channel belongs to the voltage-gated Ca2+ channel (CaV) family. "T" stands for transient, referring to the length of activation. As with other sub-types of voltage-gated Ca2+ channels, the α1 subunit is the one that determines most of the channel's properties. T-type calcium channels may contain one of three α1 subunits, α1G (CaV3.1), α1H (CaV3.2) or α1I (CaV3.3)1-3.
T-type Ca2+ channels are involved in the control of neuronal excitability and their gating can be modulated by a variety of redox agents4.
L-Ascorbic acid (ascorbate) is an endogenous redox agent that selectively inhibits native CaV3.2 channels in the peripheral and central neurons4.
L-Ascorbic acid has an IC50 of 6.5 µM on T-type current of rat DRG neurons, and IC50s of 10 and 25 nM on cloned CaV3.2 channels from human and rat, respectively4.
L-Ascorbic acid (#L-140) is a highly pure, synthetic, and biologically active compound.
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