Synaptic transmission is triggered by presynaptic calcium influx through voltage-gated calcium channels. Axon terminals of central neurons express a diverse set of homologous calcium channels, giving rise to P/Q-, N-, and R-type calcium currents. The relative contribution of these components to presynaptic calcium signalling is heterogeneous and incompletely understood. Here we report that chronic block of N-type calcium channels in developing cultured rat hippocampal neurons leads to a compensatory up-regulation of P/Q-type calcium currents. This increase was measured directly by recording whole-cell calcium currents as well as in spontaneous inhibitory postsynaptic currents, indicating a global functional up-regulation of the P/Q-component. In contrast, immunocytochemical stainings as well as quantitative real-time PCR analysis did not reveal an increased expression of Ca(v) 2.1, the underlying calcium channel alpha-subunit. We conclude that developing hippocampal neurons can compensate for the loss of one calcium current component by up-regulation of alternative isoforms at the post-translational level.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.neulet.2008.06.066 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
NYU Grossman School of Medicine, New York, NY, USA.
Background: How tauopathy disrupts direct entorhinal cortex (EC) inputs to CA1 and their plasticity is understudied, despite its critical role in memory. Moreover, dysfunction of lateral EC (LEC) input is less clear, despite its relevance to early Alzheimer's disease pathogenesis. Here we examined how tau impacts long-term potentiation (LTP) of LEC→CA1 input in a transgenic model of tauopathy.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of Arizona, Tucson, AZ, USA.
Background: Cerebral microvascular dysfunction and nitro-oxidative stress are present in patients with Alzheimer's disease (AD) and may contribute to disease progression and severity. A pro-nitro-oxidative environment can lead to post-translational modifications of ion channels central to microvascular regulation in the brain, including the large conductance Ca-activated K channels (BK). Nitro-oxidative modulation of BK can resulting in decreased activity and vascular hyper-contractility, thus compromising neurovascular regulation.
View Article and Find Full Text PDFMitochondrial calcium uniporter complex: An emerging therapeutic target for cardiovascular diseases (Review).
Int J Mol Med
March 2025
Department of Cardiology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan 421000, P.R. China.
Cardiovascular disease (CVD) is currently a major factor affecting human physical and mental health. In recent years, the relationship between intracellular Ca and CVD has been extensively studied. Ca movement across the mitochondrial inner membrane plays a vital role as an intracellular messenger, regulating energy metabolism and calcium homeostasis.
View Article and Find Full Text PDFFunctional large-conductance calcium and voltage-gated potassium channels in extracellular vesicles act as gatekeepers of structural and functional integrity.
Nat Commun
January 2025
Department of Molecular Cellular and Developmental Biology, The Ohio State University, Columbus, OH, USA.
Extracellular vesicles (EVs) are associated with intercellular communications, immune responses, viral pathogenicity, cardiovascular diseases, neurological disorders, and cancer progression. EVs deliver proteins, metabolites, and nucleic acids into recipient cells to effectively alter their physiological and biological response. During their transportation from the donor to the recipient cell EVs face differential ionic concentrations, which can be detrimental to their integrity and impact their cargo content.
View Article and Find Full Text PDFG-quadruplex stabilization provokes DNA breaks in human PKD1, revealing a second hit mechanism for ADPKD.
Nat Commun
January 2025
Department of Biomedical Sciences, Western Michigan University Homer Stryker MD School of Medicine, Kalamazoo, MI, USA.
The "secondhit" pathway is responsible for biallelic inactivation of many tumor suppressors, where a pathogenic germline allele is joined by somatic mutation of the remaining functional allele. The mechanisms are unresolved, but the human PKD1 tumor suppressor is a good experimental model for identifying the molecular determinants. Inactivation of PKD1 results in autosomal dominant polycystic kidney disease, a very common disorder characterized by the accumulation of fluid-filled cysts and end-stage renal disease.
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!