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Molecular Mechanisms of Subtype-Specific Inhibition of Neuronal T-Type Calcium Channels by Ascorbate
TLDR
This study represents the first mechanistic demonstration of ion channel modulation by ascorbate, and suggests that ascorBate may function as an endogenous modulator of neuronal excitability. Expand
A Molecular Determinant of Nickel Inhibition in Cav3.2 T-type Calcium Channels*
TLDR
Findings indicate that His-191 in the S3–S4 loop is a critical residue conferring nickel block to Cav3.3.2 and reveal a novel role for the S4 loop to control ion permeation through T-type Ca2+ channels. Expand
A Post-Burst Afterdepolarization Is Mediated by Group I Metabotropic Glutamate Receptor-Dependent Upregulation of Cav2.3 R-Type Calcium Channels in CA1 Pyramidal Neurons
The excitability of hippocampal pyramidal neurons is regulated by activation of metabotropic glutamate receptors, an effect that is mediated by modulation of R-type calcium channels.
Reducing Agents Sensitize C-Type Nociceptors by Relieving High-Affinity Zinc Inhibition of T-Type Calcium Channels
TLDR
It is demonstrated that reducing agents as well as endogenous metal chelators sensitize C-type dorsal root ganglion nociceptors by chelating Zn2+ ions off specific extracellular histidine residues on Cav3.2 T-channels, thus relieving tonic channel inhibition, enhancing Cav3-2 currents, and lowering the threshold for nocICEptor excitability in vitro and in vivo. Expand
Structural Determinants of the High Affinity Extracellular Zinc Binding Site on Cav3.2 T-type Calcium Channels*
TLDR
The key findings of the study are that the metal binding site is composed of a Asp-Gly-His motif in IS3–S4 and a second aspartate residue in IS2. Expand
Zinc Activates TREK-2 Potassium Channel Activity
TLDR
Stimulation by Zn2+ may be used as a criterion of TREK-2, distinguishing it from other two-pore K+ channels. Expand
Activation of protein kinase C augments T‐type Ca2+ channel activity without changing channel surface density
TLDR
PMA modulation of the activities of Cav3.2 T‐type channels reconstituted in Xenopus oocytes and the underlying mechanism is compared, indicating that PMA augmented T‐ type channel currents via activation of oocyte PKC. Expand
Histidine residues in the IS3–IS4 loop are critical for nickel‐sensitive inhibition of the Cav2.3 calcium channel
TLDR
It is suggested that both H179 and H183 in the IS3–IS4 loop are essential structural determinants required for nickel sensitive inhibition of the Cav2.3.2 T‐type Ca2+ channel. Expand
Molecular identification of Ca(2+)channels in human sperm
TLDR
It is proposed that not only T-type but also non-L-type calcium channels may be major gates for the external calcium influx, required for the acrosome reaction of mammalian spermatozoa. Expand
Augmentation of Cav3.2 T-Type Calcium Channel Activity by cAMP-Dependent Protein Kinase A
TLDR
Using chimeric channels constructed by replacing individual cytoplasmic loops of Cav3.2 with those of the Nav1.4 channel, which is insensitive to PKA, a region required for the PKA-mediated augmentation to the II-III loop of the Cav 3.2 channels was localized. Expand
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