ArticleNeurochemical research2015
Actin filament reorganization in astrocyte networks is a key functional step in neuroinflammation resulting in persistent pain: novel findings on network restoration.
Article in Neurochemical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 29 citations in OpenAlex.
- CHI3L1: An Emerging Player in Neuroinflammation and Neurodegeneration.Molecular neurobiology · 2025Review
- Connexin 43: An Interface Connecting Neuroinflammation to Depression.Molecules (Basel, Switzerland) · 2023Review
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- Targetability of the neurovascular unit in inflammatory diseases of the central nervous system.Immunological reviews · 2022Review
- Astrocyte Reaction to Catechol-Induced Cytotoxicity Relies on the Contact with Microglia Before Isolation.Neurotoxicity research · 2022Article
- Article
- Article
- Pressure-Induced Changes in Astrocyte GFAP, Actin, and Nuclear Morphology in Mouse Optic Nerve.Investigative ophthalmology & visual science · 2020Article
- The Importance and Control of Low-Grade Inflammation Due to Damage of Cellular Barrier Systems That May Lead to Systemic Inflammation.Frontiers in neurology · 2019Review
- Anti-inflammatory effects induced by pharmaceutical substances on inflammatory active brain astrocytes-promising treatment of neuroinflammation.Journal of neuroinflammation · 2018Article
- In vivo spatiotemporal dynamics of NG2 glia activity caused by neural electrode implantation.Biomaterials · 2018Article
- Enteric glia regulate gut motility in health and disease.Brain research bulletin · 2018Review
- Biochemical alterations in inflammatory reactive chondrocytes: evidence for intercellular network communication.Heliyon · 2018Article
- Transcriptome Analysis Reveals Neuroprotective aspects of Human Reactive Astrocytes induced by Interleukin 1β.Scientific reports · 2017Article
- Article
- Therapeutic innovation: Inflammatory-reactive astrocytes as targets of inflammation.IBRO reports · 2016Article
- Coupled cell networks are target cells of inflammation, which can spread between different body organs and develop into systemic chronic inflammation.Journal of inflammation (London, England) · 2015Review
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In recent years, the importance of glial cell activation in the generation and maintenance of long-term pain has been investigated. One novel mechanism underlying long-lasting pain is injury-induced inflammation in the periphery, followed by microglial activation in the dorsal horn of the spinal cord, which results in local neuroinflammation. An increase in neuronal excitability may follow, with intense signaling along the pain tracts to the thalamus and the parietal cortex along with other cortical regions for the identification and recognition of the injury. If the local neuroinflammation develops into a pathological state, then the astrocytes become activated. Previous studies in which lipopolysaccharide (LPS) was used to induce inflammation have shown that in a dysfunctional astrocyte network, the actin cytoskeleton is reorganized from the normally occurring F-actin stress fibers into the more diffusible, disorganized, ring-form globular G-actin. In addition, Ca(2+) signaling systems are altered, Na(+)- and glutamate transporters are downregulated, and pro-inflammatory cytokines, particularly IL-1β, are released in dysfunctional astrocyte networks. In a series of experiments, we have demonstrated that these LPS-induced changes in astrocyte function can be restored by stimulation of Gi/o and inhibition of Gs with a combination of a μ-receptor agonist and ultralow concentrations of a μ-receptor antagonist and by inhibition of cytokine release, particularly IL-1β, by the antiepileptic drug levetiracetam. These findings could be of clinical significance and indicate a novel treatment for long-term pain.
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