The roles of fractalkine/CX3CR1 system in neuronal death following pilocarpine-induced status epilepticus
Abstract
Although fractalkine is one of chemokines involved in mediation of neuronal/microglial interaction, it is not known whether fractalkine/CX3CR1-mediated pathogenesis occurs in the rat brain following epileptogenic insults. In order to elucidate the roles of the fractalkine/CX3CR1 system in microglial activation and neurodegeneration induced by status epilepticus (SE), we investigated changes in fractalkine/CX3CR1 system within the rat hippocampus following SE. In non-SE induced animals, fractalkine and CX3CR1 immunoreactivity was detected in neurons and microglia, respectively. Following SE, fractalkine immunoreactivity was transiently increased in neurons and astrocytes. CX3CR1 immunoreactivity was also transiently detected in neurons (particularly in CA1 pyramidal cells). Intracerebroventricular infusions of recombinant rat fractalkine aggravated SE-induced neuronal damage, while fractalkine IgG or CX3CR1 IgG infusion alleviated it, compared to saline-infused animals. These findings suggest that fractalkine/CX3CR1 system may play an important role in SE-induced neuronal damages via neuron-microglial interactions.
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In Yeo et al., nearly 100% of the Cx3cr1-positive cells were astrocytes.
“Nearly 100% of the Cx3cr1-positive cells were astrocytes.”
From Targeting Microglia Using Cx3cr1-Cre Lines: Revisiting the Specificity (2019) · cites this paper as Yeo et al. (2011)
Yeo et al. (2011) reported that pilocarpine-triggered SE induced very moderate expression of Cx3cr1 in astrocytes.
“Yeo et al. (2011) reported that pilocarpine-triggered SE induced very moderate expression of Cx3cr1 in astrocytes, but again the IHC data are puzzling.”
From Targeting Microglia Using Cx3cr1-Cre Lines: Revisiting the Specificity (2019) · cites this paper as Yeo et al. (2011)
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Microglia in Epilepsy: From Molecular Mechanism to Therapeutic Strategy
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Factors in glutamate excitotoxicity, inflammation and epilepsy
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- Authors
- Yeo, S.-I., Kim, J.-E., Ryu, H. J., Seo, C. H., Lee, B. C., Choi, I.-G., Kim, D.-S., & Kang, T.-C.
- Affiliations
- Hallym University (KR)
- Soonchunhyang University (KR)
- Venue
- Journal of Neuroimmunology
- Publisher
- Elsevier BV
- Published
- 2011-05
- Volume
- 234
- Issue
- 1-2
- Pages
- 93-102
- ISSN
- 0165-5728 (ISSN-L)
- OpenAlex
- W2015776364
- Cited by
- 55
- References
- 49
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 2 · 2023: 9 · 2022: 9 · 2021: 4 · 2020: 1 · 2019: 3 · 2018: 4 · 2017: 1 · 2016: 2 · 2015: 2 · 2014: 2 · 2013: 3 · 2012: 3
- FWCI
- 1.41
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neuroimmunology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Korea Healthcare technology R&D Project, Ministry for Health, Welfare and Family Affairs, Republic of Korea (A084589)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Epilepsy research and treatment
- Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
- Keywords
- fractalkine, CX3CR1, status epilepticus, pilocarpine-induced epilepsy, neuronal cell death, microglial activation, hippocampus, CA1 pyramidal neurons, astrocytes, neurodegeneration, chemokines
- MeSH terms
- CX3C Chemokine Receptor 1, Animals, Cell Count, Disease Models, Animal, Fluoresceins, Glial Fibrillary Acidic Protein, Glycoproteins, Hippocampus, Immunoglobulin G, Injections, Intraventricular, Neurons, Organic Chemicals, Pilocarpine, Status Epilepticus, Time Factors, Rats, Sprague-Dawley, Receptors, Chemokine, Lectins, Rats, Versicans, Chemokine CX3CL1
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