| Downregulation of Cav3.1 T-type Calcium Channel Expression in Age-related Hearing Loss Model. | Downregulation of Cav3.1 T-type Calcium Channel Expression in Age-related Hearing Loss Model.
Pan CC, Du ZH, Zhao Y, Chu HQ, Sun JW. | 01/8/2022 |
| Homeostatic plasticity and burst activity are mediated by hyperpolarization-activated cation currents and T-type calcium channels in neuronal cultures. | Homeostatic plasticity and burst activity are mediated by hyperpolarization-activated cation currents and T-type calcium channels in neuronal cultures.
Rátkai A, Tárnok K, Aouad HE, Micska B, Schlett K, Szücs A., Free PMC Article | 11/13/2021 |
| Concomitant genetic ablation of L-type Cav1.3 (alpha1D) and T-type Cav3.1 (alpha1G) Ca(2+) channels disrupts heart automaticity. | Concomitant genetic ablation of L-type Ca(v)1.3 (α(1D)) and T-type Ca(v)3.1 (α(1G)) Ca(2+) channels disrupts heart automaticity.
Baudot M, Torre E, Bidaud I, Louradour J, Torrente AG, Fossier L, Talssi L, Nargeot J, Barrère-Lemaire S, Mesirca P, Mangoni ME., Free PMC Article | 03/13/2021 |
| Alterations in Oscillatory Behavior of Central Medial Thalamic Neurons Demonstrate a Key Role of CaV3.1 Isoform of T-Channels During Isoflurane-Induced Anesthesia. | Alterations in Oscillatory Behavior of Central Medial Thalamic Neurons Demonstrate a Key Role of CaV3.1 Isoform of T-Channels During Isoflurane-Induced Anesthesia.
Timic Stamenic T, Feseha S, Valdez R, Zhao W, Klawitter J, Todorovic SM., Free PMC Article | 10/24/2020 |
| Adult loss of Cacna1a in mice recapitulates childhood absence epilepsy by distinct thalamic bursting mechanisms. | Adult loss of Cacna1a in mice recapitulates childhood absence epilepsy by distinct thalamic bursting mechanisms.
Miao QL, Herlitze S, Mark MD, Noebels JL., Free PMC Article | 08/22/2020 |
| T-type channels Cav3.1and Cav3.2 do not contribute to baseline blood pressure levels and ANG II-induced hypertension. Cav3.1, but not Cav3.2, contributes to aldosterone secretion. Aldosterone promotes cardiac hypertrophy during hypertension. | Deficiency of T-type Ca(2+) channels Ca(v)3.1 and Ca(v)3.2 has no effect on angiotensin II-induced hypertension but differential effect on plasma aldosterone in mice.
Thuesen AD, Finsen SH, Rasmussen LL, Andersen DC, Jensen BL, Hansen PBL. | 03/21/2020 |
| Loss of Cav3.1 makes the beating rates of the heart in vivo and perfused hearts ex vivo, as well as sinoatrial node cells, less sensitive to beta-adrenergic stimulation. | Increasing T-type calcium channel activity by β-adrenergic stimulation contributes to β-adrenergic regulation of heart rates.
Li Y, Zhang X, Zhang C, Zhang X, Li Y, Qi Z, Szeto C, Tang M, Peng Y, Molkentin JD, Houser SR, Xie M, Chen X., Free PMC Article | 08/24/2019 |
| Results confirm the idea that T-channels critically support rebound burst firing following periods of membrane hyperpolarization, similar to those that occur during inhibitory synaptic potentials in the ventral tegmental area. Behavioral results indicate that deletion of CaV3.1 channels disrupts the hyperlocomotion. | Ca(V)3.1 isoform of T-type calcium channels supports excitability of rat and mouse ventral tegmental area neurons.
Tracy ME, Tesic V, Stamenic TT, Joksimovic SM, Busquet N, Jevtovic-Todorovic V, Todorovic SM., Free PMC Article | 02/23/2019 |
| Cav3.1 expression was significantly reduced in aortae from aged compared to young WT mice. The level of phosphorylated eNOS was significantly increased in aortae from aged Cav3.1-/- mice. Cav3.1-deficient mice develop less age-dependent endothelial dysfunction. | Deletion of T-type calcium channels Ca(v)3.1 or Ca(v)3.2 attenuates endothelial dysfunction in aging mice.
Thuesen AD, Andersen K, Lyngsø KS, Burton M, Brasch-Andersen C, Vanhoutte PM, Hansen PBL. | 01/26/2019 |
| FMOD affected the expressions of the Cav1.1 and Cav3.1 genes. FMOD regulates calcium channel activity. The mRNA expressions of Cav1.1 and Cav3.1 increased during muscle regeneration. | Fibromodulin modulates myoblast differentiation by controlling calcium channel.
Lee EJ, Nam JH, Choi I. | 12/22/2018 |
| Membrane-protein extraction and use of an intracellular protein-transport inhibitor showed that GDF-15 promoted CaV3.1 and CaV3.3 alpha-subunit expression by trafficking to the membrane. | Growth differentiation factor-15 promotes glutamate release in medial prefrontal cortex of mice through upregulation of T-type calcium channels.
Liu DD, Lu JM, Zhao QR, Hu C, Mei YA., Free PMC Article | 05/5/2018 |
| Cacna1g exclusively expressed in serosal PDGFRalpha+ cells is a new pathological marker for gastrointestinal diseases. | Transcriptome analysis of PDGFRα+ cells identifies T-type Ca2+ channel CACNA1G as a new pathological marker for PDGFRα+ cell hyperplasia.
Ha SE, Lee MY, Kurahashi M, Wei L, Jorgensen BG, Park C, Park PJ, Redelman D, Sasse KC, Becker LS, Sanders KM, Ro S., Free PMC Article | 10/14/2017 |
| Data, including data from studies using knockout mice, suggest that acetylcholine- (Ach-)induced vasorelaxation/vasodilatation of intrapulmonary arteries is reduced in pulmonary hypertension, but is still dependent on Cav3.1 activity; thus, Cav3.1 contributes to intrapulmonary vascular reactivity by controlling calcium signaling in arterial endothelium and Ach-induced vasorelaxation/vasodilatation. | T-type voltage gated calcium channels are involved in endothelium-dependent relaxation of mice pulmonary artery.
Gilbert G, Courtois A, Dubois M, Cussac LA, Ducret T, Lory P, Marthan R, Savineau JP, Quignard JF. | 07/29/2017 |
| These results provide support for Cacna1g as an epilepsy modifier gene and suggest that modulation of Cav3.1 may be an effective therapeutic strategy. | Cacna1g is a genetic modifier of epilepsy caused by mutation of voltage-gated sodium channel Scn2a.
Calhoun JD, Hawkins NA, Zachwieja NJ, Kearney JA., Free PMC Article | 06/3/2017 |
| Localized Cav3.1 knockdown in the medial septum selectively enhanced object exploration, whereas the null mutant (KO) mice showed enhanced-object exploration as well as open-field exploration. | Medial septal GABAergic projection neurons promote object exploration behavior and type 2 theta rhythm.
Gangadharan G, Shin J, Kim SW, Kim A, Paydar A, Kim DS, Miyazaki T, Watanabe M, Yanagawa Y, Kim J, Kim YS, Kim D, Shin HS., Free PMC Article | 01/28/2017 |
| GluA4 subunits are required to produce an EPSC-triggerable postsynaptic action potentials after the presynaptic action potential, while Cav3.1 expression is needed to establish the driver function of L5B-POm synapses at hyperpolarized membrane potentials | Ionotropic glutamate receptor GluA4 and T-type calcium channel Cav 3.1 subunits control key aspects of synaptic transmission at the mouse L5B-POm giant synapse.
Seol M, Kuner T., Free PMC Article | 10/22/2016 |
| Mice deficient for CaV3.1 were resistant to the induction of experimental autoimmune encephalomyelitis and had reduced productions of the granulocyte-macrophage colony-stimulating factor by central nervous system-infiltrating Th1 and Th17 cells. | Low-Voltage-Activated CaV3.1 Calcium Channels Shape T Helper Cell Cytokine Profiles.
Wang H, Zhang X, Xue L, Xing J, Jouvin MH, Putney JW, Anderson MP, Trebak M, Kinet JP., Free PMC Article | 10/1/2016 |
| Cross-frequency coupling between low-frequency and gamma rhythms was pronounced in wild-type but not in CaV3.1 knockouts, suggesting that the presence of CaV3.1 channels is a key element in the pathophysiology of trigeminal neuropathic pain. | Pathophysiological implication of CaV3.1 T-type Ca2+ channels in trigeminal neuropathic pain.
Choi S, Yu E, Hwang E, Llinás RR., Free PMC Article | 07/30/2016 |
| Results suggest that alpha1G T-type calcium channel plays a modulatory role in the duration and frequency of hippocampal seizures as well as the epileptogenicity of kainic acid-induced temporal lobe epilepsy in mice, mostly during acute periods | Cav3.1 T-type calcium channel modulates the epileptogenicity of hippocampal seizures in the kainic acid-induced temporal lobe epilepsy model.
Kim CH. | 06/4/2016 |
| CaV3.1 and CaV3.2 are substrates for EHD3-dependent protein trafficking in heart | Eps15 Homology Domain-containing Protein 3 Regulates Cardiac T-type Ca2+ Channel Targeting and Function in the Atria.
Curran J, Musa H, Kline CF, Makara MA, Little SC, Higgins JD, Hund TJ, Band H, Mohler PJ., Free PMC Article | 08/8/2015 |
| This study reported on the cloning and characterization of a proximal promoter region and initiated the analysis of transcription factors that control CaV 3.1 channel expression using the murine Cacna1g gene as a model. | Transcription factor Sp1 regulates T-type Ca(2+) channel CaV 3.1 gene expression.
González-Ramírez R, Martínez-Hernández E, Sandoval A, Felix R. | 03/29/2014 |
| Ca(v)3.1-dependent synaptic depression at thalamocortical projections contributes to mechanisms of forward suppression in the auditory cortex | 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.
Bayazitov IT, Westmoreland JJ, Zakharenko SS., Free PMC Article | 02/1/2014 |
| Suggest that T-type Ca(2+) channels play an important role in infranodal escape automaticity. | T-type calcium current contributes to escape automaticity and governs the occurrence of lethal arrhythmias after atrioventricular block in mice.
Le Quang K, Benito B, Naud P, Qi XY, Shi YF, Tardif JC, Gillis MA, Dobrev D, Charpentier F, Nattel S. | 11/30/2013 |
| CaV 3.1 channels are important for the myogenic tone at low arterial pressure, which is potentially relevant under resting conditions in vivo mice. | Myogenic tone is impaired at low arterial pressure in mice deficient in the low-voltage-activated CaV 3.1 T-type Ca(2+) channel.
Björling K, Morita H, Olsen MF, Prodan A, Hansen PB, Lory P, Holstein-Rathlou NH, Jensen LJ. | 09/28/2013 |
| Ca(v)3.1 is required for vascular smooth muscle proliferation during neointimal formation, and blocking of Ca(v)3.1 may be beneficial for preventing restenosis. | The Ca(v)3.1 T-type calcium channel is required for neointimal formation in response to vascular injury in mice.
Tzeng BH, Chen YH, Huang CH, Lin SS, Lee KR, Chen CC. | 04/27/2013 |