ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
Induction of interleukin-6 by depolarization of neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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Who cites it
48 citing papers in PubMed, 119 citations in OpenAlex.
- The immune-microbiome axis in salt-sensitive hypertension: a focus on renal and neural mechanisms.Frontiers in physiology · 2025Review
- The Role of IL-6 in Neurodegenerative Disorders.Neurochemical research · 2024Review
- A suitable model to investigate acute neurological consequences of coronavirus infection.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Cortical Spreading Depolarization and Delayed Cerebral Ischemia; Rethinking Secondary Neurological Injury in Subarachnoid Hemorrhage.International journal of molecular sciences · 2023Review
- Neuroinflammatory mediators in acquired epilepsy: an update.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Review
- Intermittent hypoxia: linkage between OSAS and epilepsy.Frontiers in pharmacology · 2023Review
- Microglial diversity along the hippocampal longitudinal axis impacts synaptic plasticity in adult male mice under homeostatic conditions.Journal of neuroinflammation · 2022Article
- An integrated cytokine and kynurenine network as the basis of neuroimmune communication.Frontiers in neuroscience · 2022Review
- Article
- Pathomechanism Characterization and Potential Therapeutics Identification for Parkinson's Disease Targeting Neuroinflammation.International journal of molecular sciences · 2021Article
- Neuroinflammation in Post-Traumatic Epilepsy: Pathophysiology and Tractable Therapeutic Targets.Brain sciences · 2019Review
- Increased IL-6 expression in astrocytes is associated with emotionality, alterations in central amygdala GABAergic transmission, and excitability during alcohol withdrawal.Brain, behavior, and immunity · 2019Article
- Anti-inflammatory and antioxidant effects of muscarinic acetylcholine receptor (mAChR) activation in the rat hippocampus.Scientific reports · 2019Article
- Article
- ATM inhibition prevents interleukin-6 from contributing to the proliferation of glioblastoma cells after ionizing radiation.Journal of neuro-oncology · 2018Article
- Tb II-I, a Fraction Isolated fromToxins · 2018Article
- AMPA-ergic regulation of amyloid-β levels in an Alzheimer's disease mouse model.Molecular neurodegeneration · 2018Article
- Inflammatory Signaling in Hypertension: Regulation of Adrenal Catecholamine Biosynthesis.Frontiers in endocrinology · 2018Review
- Spinal activity of interleukin 6 mediates myelin basic protein-induced allodynia.Brain, behavior, and immunity · 2016Article
- Transgenic mice with increased astrocyte expression of IL-6 show altered effects of acute ethanol on synaptic function.Neuropharmacology · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin-6 (IL-6) has neuromodulatory and neuroprotective effects in vivo. It is expressed in glial cells and neurons both under physiological conditions and in various neurological diseases. Although the expression of IL-6 in glia has been intensely investigated, little is known about the regulation of IL-6 production by neurons. Therefore, we investigated the regulation of IL-6 expression in neurons. Membrane depolarization raised IL-6 mRNA accumulation in primary cortical cells and the PC-12 cell line. In vivo, IL-6 mRNA in the brain increased significantly after epileptic seizures. To investigate IL-6 gene transcription, PC-12 cells were transfected with reporter gene constructs containing the human IL-6 promoter. Membrane depolarization raised IL-6 transcription twofold to fourfold. This increase could be blocked by lowering extracellular Ca(2+) levels or by inhibiting L-type Ca(2+) channels or Ca(2+)/calmodulin-dependent protein kinases. Internal mutations in various elements of the IL-6 promoter revealed the glucocorticoid response element (GRE) 2 to be a depolarization-responsive element. Although the GRE2 bound the glucocorticoid receptor (GR) and was stimulated by dexamethasone, the GR was not responsible for the effect of membrane depolarization because a consensus GRE did not mediate stimulation by membrane depolarization. Instead, another yet undefined factor that binds to the IL-6 GRE2 may mediate the response to membrane depolarization. These data demonstrate that the expression of IL-6 in neurons is regulated by membrane depolarization and suggest a novel Ca(2+)-responsive promoter element. Through this mechanism, IL-6 may function as a neuromodulator induced by neuronal activity.
Indexed as
Identifiers
11102468PMC6773078W2888001539What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.