ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Selective T-type calcium channel block in thalamic neurons reveals channel redundancy and physiological impact of I(T)window.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers, 1 of them a synthesis that pooled it.
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Who cites it
131 citing papers in PubMed, 1 synthesis or guideline pooled it, 196 citations in OpenAlex.
- Analysing an allelic series of rare missense variants of CACNA1I in a Swedish schizophrenia cohort.Brain : a journal of neurology · 2022Pooled it
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- Parvalbumin and Somatostatin Neurons in the Thalamic Reticular Nucleus Modulate Visual Information Processing in V1 of Mouse.Neuroscience bulletin · 2025Article
- Extremely low-frequency electromagnetic fields facilitate proliferation and functional differentiation in spinal neural stem cells.Scientific reports · 2025Article
- Axon initial segment structure and function in health and disease.Physiological reviews · 2025Review
- Thalamocortical Dynamics during Rapid Eye Movement Sleep in the Mouse Somatosensory Pathway.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- T-Type CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Spike-and-wave discharges of absence seizures in a sleep waves-constrained corticothalamic model.CNS neuroscience & therapeutics · 2024Article
- Article
- T-type CaCell reports · 2023Article
- T-type calcium channels as therapeutic targets in essential tremor and Parkinson's disease.Annals of clinical and translational neurology · 2023Review
- CaNeuropharmacology · 2023Article
- Sex-specific hypnotic effects of the neuroactive steroid (3β,5β,17β)-3-hydroxyandrostane-17-carbonitrile are mediated by peripheral metabolism into an active hypnotic steroid.British journal of anaesthesia · 2023Article
- CaHandbook of experimental pharmacology · 2023Article
- The Role of Voltage-Gated Calcium Channels in Basal Ganglia Neurodegenerative Disorders.Current neuropharmacology · 2023Review
- µ-Theraphotoxin Pn3a inhibition of CaeLife · 2022Article
- Human midbrain dopaminergic neuronal differentiation markers predict cell therapy outcomes in a Parkinson's disease model.The Journal of clinical investigation · 2022Article
- Focused ultrasound excites cortical neurons via mechanosensitive calcium accumulation and ion channel amplification.Nature communications · 2022Article
- The T-Type Calcium Channel Cav3.2 in Somatostatin Interneurons in Spinal Dorsal Horn Participates in Mechanosensation and Mechanical Allodynia in Mice.Frontiers in cellular neuroscience · 2022Article
71 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 4 countries.
Funding
Abstract
Although it is well established that low-voltage-activated T-type Ca(2+) channels play a key role in many neurophysiological functions and pathological states, the lack of selective and potent antagonists has so far hampered a detailed analysis of the full impact these channels might have on single-cell and neuronal network excitability as well as on Ca(2+) homeostasis. Recently, a novel series of piperidine-based molecules has been shown to selectively block recombinant T-type but not high-voltage-activated (HVA) Ca(2+) channels and to affect a number of physiological and pathological T-type channel-dependent behaviors. Here we directly show that one of these compounds, 3,5-dichloro-N-[1-(2,2-dimethyl-tetrahydro-pyran-4-ylmethyl)-4-fluoro-piperidin-4-ylmethyl]-benzamide (TTA-P2), exerts a specific, potent (IC(50) = 22 nm), and reversible inhibition of T-type Ca(2+) currents of thalamocortical and reticular thalamic neurons, without any action on HVA Ca(2+) currents, Na(+) currents, action potentials, and glutamatergic and GABAergic synaptic currents. Thus, under current-clamp conditions, the low-threshold Ca(2+) potential (LTCP)-dependent high-frequency burst firing of thalamic neurons is abolished by TTA-P2, whereas tonic firing remains unaltered. Using TTA-P2, we provide the first direct demonstration of the presence of a window component of Ca(2+) channels in neurons and its contribution to the resting membrane potential of thalamic neurons and to the Up state of their intrinsically generated slow (<1 Hz) oscillation. Moreover, we demonstrate that activation of only a small fraction of the T-type channel population is required to generate robust LTCPs, suggesting that LTCP-driven bursts of action potentials can be evoked at depolarized potentials where the vast majority of T-type channels are inactivated.
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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.