ArticleBiophysical journal2000
pH modification of human T-type calcium channel gating.
Article in Biophysical journal, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 47 citations in OpenAlex.
- Role of the C-terminal domain in modifying pH-dependent regulation of CaChannels (Austin, Tex.) · 2025Article
- Electrophysiological characterization of a CaMolecular brain · 2023Article
- Investigation ofFrontiers in molecular neuroscience · 2022Article
- Peripheral Inflammation Results in Increased Excitability of Capsaicin-Insensitive Nociceptive DRG Neurons Mediated by Upregulation of ASICs and Voltage-Gated Ion Channels.Frontiers in cellular neuroscience · 2021Article
- Low pH Attenuates Apoptosis by Suppressing the Volume-Sensitive Outwardly Rectifying (VSOR) Chloride Current in Chondrocytes.Frontiers in cell and developmental biology · 2021Article
- Two sets of amino acids of the domain I of Cav2.3 Ca(2+) channels contribute to their high sensitivity to extracellular protons.Pflugers Archiv : European journal of physiology · 2011Article
- Regulation of cardiac Ca(2+) channel by extracellular Na(+).Cell calcium · 2011Article
- Genetic enhancement of thalamocortical network activity by elevating alpha 1g-mediated low-voltage-activated calcium current induces pure absence epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Extracellular proton modulates GABAergic synaptic transmission in rat hippocampal CA3 neurons.Brain research · 2007Article
- Role of Domain IV/S4 outermost arginines in gating of T-type calcium channels.Pflugers Archiv : European journal of physiology · 2005Article
- Elevated thalamic low-voltage-activated currents precede the onset of absence epilepsy in the SNAP25-deficient mouse mutant coloboma.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Modulation and pharmacology of low voltage-activated ("T-Type") calcium channels.Journal of bioenergetics and biomembranes · 2003Review
- Mechanisms of H+ modulation of glycinergic response in rat sacral dorsal commissural neurons.The Journal of physiology · 2003Article
- Conotoxins as sensors of local pH and electrostatic potential in the outer vestibule of the sodium channel.The Journal of general physiology · 2003Article
- Monovalent cations contribute to T-type calcium channel (Cav3.1 and Cav3.2) selectivity.The Journal of membrane biology · 2003Article
- Pore structure influences gating properties of the T-type Ca2+ channel alpha1G.The Journal of general physiology · 2003Article
- Extracellular Ca2+ modulates the effects of protons on gating and conduction properties of the T-type Ca2+ channel alpha1G (CaV3.1).The Journal of general physiology · 2003Article
- Mutations in high-voltage-activated calcium channel genes stimulate low-voltage-activated currents in mouse thalamic relay neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
External pH (pH(o)) modifies T-type calcium channel gating and permeation properties. The mechanisms of T-type channel modulation by pH remain unclear because native currents are small and are contaminated with L-type calcium currents. Heterologous expression of the human cloned T-type channel, alpha1H, enables us to determine the effect of changing pH on isolated T-type calcium currents. External acidification from pH(o) 8.2 to pH(o) 5.5 shifts the midpoint potential (V(1/2)) for steady-state inactivation by 11 mV, shifts the V(1/2) for maximal activation by 40 mV, and reduces the voltage dependence of channel activation. The alpha1H reversal potential (E(rev)) shifts from +49 mV at pH(o) 8.2 to +36 mV at pH(o) 5.5. The maximal macroscopic conductance (G(max)) of alpha1H increases at pH(o) 5.5 compared to pH(o) 8.2. The E(rev) and G(max) data taken together suggest that external protons decrease calcium/monovalent ion relative permeability. In response to a sustained depolarization alpha1H currents inactivate with a single exponential function. The macroscopic inactivation time constant is a steep function of voltage for potentials < -30 mV at pH(o) 8.2. At pH(o) 5.5 the voltage dependence of tau(inact) shifts more depolarized, and is also a more gradual function of voltage. The macroscopic deactivation time constant (tau(deact)) is a function of voltage at the potentials tested. At pH(o) 5.5 the voltage dependence of tau(deact) is simply transposed by approximately 40 mV, without a concomitant change in the voltage dependence. Similarly, the delay in recovery from inactivation at V(rec) of -80 mV in pH(o) 5.5 is similar to that with a V(rec) of -120 mV at pH(o) 8.2. We conclude that alpha1H is uniquely modified by pH(o) compared to other calcium channels. Protons do not block alpha1H current. Rather, a proton-induced change in activation gating accounts for most of the change in current magnitude with acidification.
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