ArticleThe journal of physiological sciences : JPS2012
Interleukin-6 inhibits L-type calcium channel activity of cultured cerebellar granule neurons.
Article in The journal of physiological sciences : JPS, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 23 citations in OpenAlex.
- IL-6 Does Not Influence the Expression ofInternational journal of molecular sciences · 2024Article
- Review
- Immune-Triggered Forms of Plasticity Across Brain Regions.Frontiers in cellular neuroscience · 2022Review
- Alcohol alters IL-6 Signal Transduction in the CNS of Transgenic Mice with Increased Astrocyte Expression of IL-6.Cellular and molecular neurobiology · 2021Article
- Alterations in the CaExploration of targeted anti-tumor therapy · 2021Article
- Glial responses to implanted electrodes in the brain.Nature biomedical engineering · 2017Article
- Altered Sodium and Potassium, but not Calcium Currents in Cerebellar Granule Cells in an In Vitro Model of Neuronal Injury.Cellular and molecular neurobiology · 2017Article
- Article
- Calcium dysregulation and neuroinflammation: discrete and integrated mechanisms for age-related synaptic dysfunction.Ageing research reviews · 2013Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Our previous work has shown that interleukin-6 (IL-6) implements its neuroprotective effect by inhibiting the intracellular Ca(2+) overload in neurons. Here, we examined whether regulation of L-type calcium channels (LCCs) activities is involved in the neuroprotective action of IL-6. In cultured cerebellar granule neurons (CGNs), patch-clamp recording showed that the whole-cell Ca(2+) current and LCC current were significantly reduced by IL-6 pretreatment (120 ng/ml, for 24 h). Calcium imaging data indicated that IL-6 significantly suppressed high K(+)-induced intracellular Ca(2+) overload and LCC Ca(2+) influx. Moreover, expression of the LCC subunit, Ca(v)1.2, was remarkably downregulated by IL-6 in cultured CGNs. These findings suggest that IL-6 exerts a neurotrophic effect by preventing Ca(2+) overload, at least partly through inhibition of LCC activity in cultured CGNs.
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