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Chemokine CCL2 and its receptor CCR2 are increased in the hippocampus following pilocarpine-induced status epilepticus. | LitMetric

AI Article Synopsis

  • Neuroinflammation linked to seizures can influence the development of epilepsy, with CCR2 and CCL2 playing key roles in monocyte infiltration during brain inflammation caused by seizures.
  • In a study, status epilepticus (SE) was induced in rats using pilocarpine, followed by analysis of CCR2 and CCL2 levels in the hippocampus through immunohistochemistry and molecular assays.
  • Results showed increased CCR2 levels and changes in expression among neurons and astrocytes in the hippocampus after SE, suggesting that these changes may contribute to harmful neuroplasticity and inflammation following seizures.

Article Abstract

Background: Neuroinflammation occurs after seizures and is implicated in epileptogenesis. CCR2 is a chemokine receptor for CCL2 and their interaction mediates monocyte infiltration in the neuroinflammatory cascade triggered in different brain pathologies. In this work CCR2 and CCL2 expression were examined following status epilepticus (SE) induced by pilocarpine injection.

Methods: SE was induced by pilocarpine injection. Control rats were injected with saline instead of pilocarpine. Five days after SE, CCR2 staining in neurons and glial cells was examined using imunohistochemical analyses. The number of CCR2 positive cells was determined using stereology probes in the hippocampus. CCL2 expression in the hippocampus was examined by molecular assay.

Results: Increased CCR2 was observed in the hippocampus after SE. Seizures also resulted in alterations to the cell types expressing CCR2. Increased numbers of neurons that expressed CCR2 was observed following SE. Microglial cells were more closely apposed to the CCR2-labeled cells in SE rats. In addition, rats that experienced SE exhibited CCR2-labeling in populations of hypertrophied astrocytes, especially in CA1 and dentate gyrus. These CCR2+ astroctytes were not observed in control rats. Examination of CCL2 expression showed that it was elevated in the hippocampus following SE.

Conclusion: The data show that CCR2 and CCL2 are up-regulated in the hippocampus after pilocarpine-induced SE. Seizures also result in changes to CCR2 receptor expression in neurons and astrocytes. These changes might be involved in detrimental neuroplasticity and neuroinflammatory changes that occur following seizures.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2804573PMC
http://dx.doi.org/10.1186/1742-2094-6-40DOI Listing

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