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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.
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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.
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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.
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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.
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Cacna1g exclusively expressed in serosal PDGFRalpha+ cells is a new pathological marker for gastrointestinal diseases.
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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.
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These results provide support for Cacna1g as an epilepsy modifier gene and suggest that modulation of Cav3.1 may be an effective therapeutic strategy.
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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.
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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
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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.
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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.
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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
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CaV3.1 and CaV3.2 are substrates for EHD3-dependent protein trafficking in heart
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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.
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Ca(v)3.1-dependent synaptic depression at thalamocortical projections contributes to mechanisms of forward suppression in the auditory cortex
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Suggest that T-type Ca(2+) channels play an important role in infranodal escape automaticity.
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CaV 3.1 channels are important for the myogenic tone at low arterial pressure, which is potentially relevant under resting conditions in vivo mice.
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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.
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Activation of Cav3.1 T-type channel subunit during wake-like states is a major determinant for single and multiple spike occurrence during tonic firing and for the robustness of the thalamocortical transfer of sensory inputs.
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Elimination of Cav3.1 expression leads to impaired cardiac function and enhanced arrhythmia vulnerability post-myocardial infarction.
