ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1991
Spreading depression increases immunohistochemical staining of glial fibrillary acidic protein.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
50 citing papers in PubMed, 173 citations in OpenAlex.
- Spreading depolarization activates the cGAS-STING pathway and drives cranial nociception: therapeutic potential of STING modulation.The journal of headache and pain · 2026Article
- Neuroinflammatory and Redox Responses in a Rat Model of NTG-Induced Migraine.International journal of molecular sciences · 2025Article
- Spreading depolarization as a therapeutic target in migraine.Nature reviews. Neurology · 2025Review
- The link between spreading depolarization and innate immunity in the central nervous system.The journal of headache and pain · 2025Review
- Cause of Death Analysis in a 9½-Year-Old with COVID-19 and Dravet Syndrome.Pathophysiology : the official journal of the International Society for Pathophysiology · 2025Article
- Chronic Hyperhomocysteinemia Impairs CSD Propagation and Induces Cortical Damage in a Rat Model of Migraine with Aura.Biomolecules · 2024Article
- The Role of Glial Cells in Different Phases of Migraine: Lessons from Preclinical Studies.International journal of molecular sciences · 2023Review
- Article
- Review
- Repeated mild traumatic brain injuries impair visual discrimination learning in adolescent mice.Neurobiology of learning and memory · 2020Article
- Stereological Analysis of Early Gene Expression Using Egr-1 Immunolabeling After Spreading Depression in the Rat Somatosensory Cortex.Frontiers in neuroscience · 2019Article
- IFNγ-Stimulated Dendritic Cell Exosomes for Treatment of Migraine Modeled Using Spreading Depression.Frontiers in neuroscience · 2019Article
- Apoptosis Following Cortical Spreading Depression in Juvenile Rats.Molecular neurobiology · 2018Article
- Intranasally administered IGF-1 inhibits spreading depression in vivo.Brain research · 2017Article
- Cortical Spreading Depression Closes Paravascular Space and Impairs Glymphatic Flow: Implications for Migraine Headache.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Review
- Phasic Treatment with Interferon Gamma Stimulates Release of Exosomes that Protect Against Spreading Depression.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2015Article
- Cortical spreading depolarization stimulates gliogenesis in the rat entorhinal cortex.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2015Article
- Spreading depression transiently disrupts myelin via interferon-gamma signaling.Experimental neurology · 2015Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Reactive astrocytosis is a process by which astrocytes respond to brain injury by showing an increase in glial fibrillary acidic protein (GFAP) staining that is associated with hypertrophy and/or hyperplasia of these cells. Because spreading depression (SD) is a perturbation uncomplicated by neuronal necrosis and is seen in both in vivo and in vitro neural structures, we sought to determine whether SD was a sufficient stimulus to induce enhanced GFAP staining. SD was elicited in anesthetized rats by application of KCI to parietal cortex for 3 hr; equimolar NaCI was applied to contralateral cortex. SD was confirmed by monitoring DC potentials in frontal neocortices. Animals were allowed to recover for 48 hr, and their brains were processed for semiquantitative and computer-based analyses of GFAP staining intensity. Experimental GFAP staining was referenced to contralateral control levels. Neocortical SD (13-37 SDs) was associated with a significant (p less than 10(-4)), 43% increase in GFAP staining intensity, which remained statistically greater than normal for more than 2 weeks. If SD was inhibited by combined hyperoxia and hypercarbia, only a nonsignificant (p greater than 0.20), 7% increase in GFAP staining was seen. Thus, SD may be a useful physiologic process with which to begin to explore the cellular mechanisms that induce the transformation of normal astrocytes into reactive species.
Indexed as
Identifiers
1906091PMC2709772W1627504329What 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.