ArticleMolecules and cells2014
Astrogliosis is a possible player in preventing delayed neuronal death.
Article in Molecules and cells, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- Plasma GFAP as a mediator and moderator of Aβ, tau, and neurodegeneration in Alzheimer's disease.NPJ dementia · 2026Article
- Mobilizing endogenous neuroprotection: the mechanism of the protective effect of acupuncture on the brain after stroke.Frontiers in neuroscience · 2024Review
- Regulation of MAP2, GFAP, and calcium in the CA3 Region Following Kainic Acid Exposure to organotypic hippocampal slice culture.F1000Research · 2023Article
- Asiatic acid attenuates aluminium chloride-induced behavioral changes, neuronal loss and astrocyte activation in rats.Metabolic brain disease · 2022Article
- Kir4.1 is coexpressed with stemness markers in activated astrocytes in the injured brain and a Kir4.1 inhibitor BaClThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2021Article
- Prenatal Hypoxia Induces Premature Aging Accompanied by Impaired Function of the Glutamatergic System in Rat Hippocampus.Neurochemical research · 2021Article
- Pacific Ciguatoxin Induces Excitotoxicity and Neurodegeneration in the Motor Cortex Via Caspase 3 Activation: Implication for Irreversible Motor Deficit.Molecular neurobiology · 2018Article
- Astrocytes, Microglia, and Parkinson's Disease.Experimental neurobiology · 2018Review
- Decreased Motor Neuron Support by SMA Astrocytes due to Diminished MCP1 Secretion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Astrocytes and Microglia as Non-cell Autonomous Players in the Pathogenesis of ALS.Experimental neurobiology · 2016Review
- Blood biomarkers for brain injury: What are we measuring?Neuroscience and biobehavioral reviews · 2016Review
- PINK1 expression increases during brain development and stem cell differentiation, and affects the development of GFAP-positive astrocytes.Molecular brain · 2016Article
- Metabolic Changes Following Perinatal Asphyxia: Role of Astrocytes and Their Interaction with Neurons.Frontiers in aging neuroscience · 2016Review
- Neurointegrity and neurophysiology: astrocyte, glutamate, and carbon monoxide interactions.Medical gas researchReview
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitigating secondary delayed neuronal injury has been a therapeutic strategy for minimizing neurological symptoms after several types of brain injury. Interestingly, secondary neuronal loss appeared to be closely related to functional loss and/or death of astrocytes. In the brain damage induced by agonists of two glutamate receptors, N-ethyl-D-aspartic acid (NMDA) and kainic acid (KA), NMDA induced neuronal death within 3 h, but did not increase further thereafter. However, in the KA-injected brain, neuronal death was not obviously detectable even at injection sites at 3 h, but extensively increased to encompass the entire hemisphere at 7 days. Brain inflammation, a possible cause of secondary neuronal damage, showed little differences between the two models. Importantly, however, astrocyte behavior was completely different. In the NMDA-injected cortex, the loss of glial fibrillary acidic protein-expressing (GFAP+) astrocytes was confined to the injection site until 7 days after the injection, and astrocytes around the damage sites showed extensive gliosis and appeared to isolate the damage sites. In contrast, in the KA-injected brain, GFAP+ astrocytes, like neurons, slowly, but progressively, disappeared across the entire hemisphere. Other markers of astrocytes, including S100β, glutamate transporter EAAT2, the potassium channel Kir4.1 and glutamine synthase, showed patterns similar to that of GFAP in both NMDA- and KA-injected cortexes. More importantly, astrocyte disappearance and/or functional loss preceded neuronal death in the KA-injected brain. Taken together, these results suggest that loss of astrocyte support to neurons may be a critical cause of delayed neuronal death in the injured brain.
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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.