ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Recovery from inactivation of t-type ca2+ channels in rat thalamic neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
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- Is Purkinje Neuron Hyperpolarisation Important for Cerebellar Synaptic Plasticity? A Retrospective and Prospective Analysis.Cerebellum (London, England) · 2020Review
- Dynamical characterization of inactivation path in voltage-gated Na(+) ion channel by non-equilibrium response spectroscopy.Channels (Austin, Tex.) · 2016Article
- Flow- and voltage-dependent blocking effect of ethosuximide on the inward rectifier K⁺ (Kir2.1) channel.Pflugers Archiv : European journal of physiology · 2015Article
- Using simultaneous voltage and calcium imaging to study fast Ca(2+) channels.Neurophotonics · 2015Article
- Imaging fast calcium currents beyond the limitations of electrode techniques.Biophysical journal · 2014Article
- T-type calcium channels promote predictive homeostasis of input-output relations in thalamocortical neurons of lateral geniculate nucleus.Frontiers in computational neuroscience · 2014Article
- Forward suppression in the auditory cortex is caused by the Ca(v)3.1 calcium channel-mediated switch from bursting to tonic firing at thalamocortical projections.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Modulation of subthalamic T-type Ca(2+) channels remedies locomotor deficits in a rat model of Parkinson disease.The Journal of clinical investigation · 2011Article
- Comparison of synaptic transmission and plasticity between sensory and cortical synapses on relay neurons in the ventrobasal nucleus of the rat thalamus.The Journal of physiology · 2010Article
- LEF1/beta-catenin complex regulates transcription of the Cav3.1 calcium channel gene (Cacna1g) in thalamic neurons of the adult brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Slow conductances could underlie intrinsic phase-maintaining properties of isolated lobster (Panulirus interruptus) pyloric neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
- Enhancement of excitatory synaptic integration by GABAergic inhibition in the subthalamic nucleus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Functional characterization and neuronal modeling of the effects of childhood absence epilepsy variants of CACNA1H, a T-type calcium channel.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Slow inactivation of the Ca(V)3.1 isotype of T-type calcium channels.The Journal of physiology · 2004Article
- Availability of low-threshold Ca2+ current in retinal ganglion cells.Journal of neurophysiology · 2003Article
- The position of the fourth segment of domain 4 determines status of the inactivation gate in Na+ channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Pore structure influences gating properties of the T-type Ca2+ channel alpha1G.The Journal of general physiology · 2003Article
- Cloning and expression of the human T-type channel Ca(v)3.3: insights into prepulse facilitation.Biophysical journal · 2002Article
- Mechanism of inactivation gating of human T-type (low-voltage activated) calcium channels.Biophysical journal · 2002Article
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2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We studied the gating kinetics, especially the kinetics of recovery from inactivation, of T-type Ca(2+) channels (T-channels) in thalamic neurons. The recovery course is associated with no discernible Ca(2+) current and is characterized by an initial delay, as well as a subsequent exponential phase. These findings are qualitatively similar to previous observations on neuronal Na(+) channels and suggest that T-channels also must deactivate to recover from inactivation. In contrast to Na(+) channels in which both the delay and the time constant of the exponential phase are shortened with increasing hyperpolarization, in T-channels the time constant of the exponential recovery phase remains unchanged between -100 and -200 mV, although the initial delay is still shortened e-fold per 43 mV hyperpolarization over the same voltage range. The deactivating kinetics of tail T-currents also show a similar voltage dependence between -90 and -170 mV. According to the hinged-lid model of fast inactivation, these findings suggest that the affinity difference between inactivating peptide binding to the activated channel and binding to the fully deactivated channel is much smaller in T-channels than in Na(+) channels. Moreover, the inactivating peptide in T-channels seems to have much slower binding and unbinding kinetics, and the unbinding rates probably remain unchanged once the inactivated T-channel has gone through the initial steps of deactivation and "closes" the pore (with the activation gate). T-channels thus might have a more rigid hinge and a more abrupt conformational change in the inactivation machinery associated with opening and closing of the pore.
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11245673PMC6762607W1669283316What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.