Calcium flux through L-type voltage-activated calcium (Cav1) channels is crucial for regulating brain functions including memory formation and behavior. Alterations in Ca²+ homeostasis have been linked to many cognitive disorders, and understanding the regulation of this process is crucial for their remedy. Therefore, here, we have evaluated the effect of a multifunctional protein known to be involved in memory functions called regulator of G-protein signaling 14 (RGS-14) on Cav1 channel activity in neuronal cell lines NG108-15 and SH-SY5Y. RGS-14 protein produced significant reduction in Ca²+ influx in both cell lines and this effect was dependent on nifedipine-sensitive Cav1 channels. Thus, our results provide evidence supporting the idea that RGS-14 may facilitate the cognitive processing by modulating Cav1 channel-mediated intracellular Ca²+ transients.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3181207 | PMC |
| http://dx.doi.org/10.1097/WNR.0b013e32833f7b7b | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
14-3-3 promotes sarcolemmal expression of cardiac Ca1.2 and nucleates isoproterenol-triggered channel superclustering.
Proc Natl Acad Sci U S A
February 2025
Department of Physiology and Membrane Biology, University of California Davis, Davis, CA 95616.
The L-type Ca channel (Ca1.2) is essential for cardiac excitation-contraction coupling. To contribute to the inward Ca flux that drives Ca-induced-Ca-release, Ca1.
View Article and Find Full Text PDFThe Protective Effect of Nimodipine in Schwann Cells Is Related to the Upregulation of LMO4 and SERCA3 Accompanied by the Fine-Tuning of Intracellular Calcium Levels.
Int J Mol Sci
January 2025
Department of Neurosurgery, Medical Faculty, Martin Luther University Halle-Wittenberg, Ernst-Grube-Straße 40, 06120 Halle (Saale), Germany.
Nimodipine is the current gold standard in the treatment of subarachnoid hemorrhage, as it is the only known calcium channel blocker that has been proven to improve neurological outcomes. In addition, nimodipine exhibits neuroprotective properties in vitro under various stress conditions. Furthermore, clinical studies have demonstrated a neuroprotective effect of nimodipine after vestibular schwannoma surgery.
View Article and Find Full Text PDFActivity dependent Clustering of Neuronal L-Type Calcium Channels by CaMKII.
bioRxiv
January 2025
Department of Molecular Physiology and Biophysics.
Neuronal excitation-transcription (E-T) coupling pathways can be initiated by local increases of Ca concentrations within a nanodomain close to the L-type voltage-gated Ca channel (LTCC). However, molecular mechanisms controlling LTCC organization within the plasma membrane that help creation these localized signaling domains remain poorly characterized. Here, we report that neuronal depolarization increases Ca1.
View Article and Find Full Text PDFExercise-induced cytosolic calcium oscillations: mechanisms and modulation of T-cell function.
Biochem Biophys Res Commun
January 2025
School of Physical Education, China University of Geosciences (Wuhan), Wuhan, China. Electronic address:
This study investigated time-dependent changes in intracellular Ca⁺ levels in T cells, regulatory mechanisms, and functional effects after acute exercise. Male C57BL/6 mice were assigned to control and exercise groups, with the latter sacrificed at different intervals post-exercise. Murine splenic lymphocytes were isolated, and cytosolic Ca⁺ levels were measured using Fluo-3/AM.
View Article and Find Full Text PDFArrhythmogenic calmodulin variants D131E and Q135P disrupt interaction with the L-type voltage-gated Ca channel (Ca1.2) and reduce Ca-dependent inactivation.
Acta Physiol (Oxf)
February 2025
Department of Biochemistry, Cell and Systems Biology, Institute of Systems, Molecular and Integrative Biology, Faculty of Health and Life Sciences, University of Liverpool, Liverpool, UK.
Aim: Long QT syndrome (LQTS) and catecholaminergic polymorphism ventricular tachycardia (CPVT) are inherited cardiac disorders often caused by mutations in ion channels. These arrhythmia syndromes have recently been associated with calmodulin (CaM) variants. Here, we investigate the impact of the arrhythmogenic variants D131E and Q135P on CaM's structure-function relationship.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!