title: 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.
authors.affiliation: Department of Anatomy and Neurobiology, College of Medicine, Hallym University, Chunchon, Kangwon-Do 200-702, South Korea.
authors.forename: S-I
authors.initials: SI
authors.lastname: Yeo
authors.forename: J-E
authors.initials: JE
authors.lastname: Kim
authors.forename: H J
authors.initials: HJ
authors.lastname: Ryu
authors.forename: C H
authors.initials: CH
authors.lastname: Seo
authors.forename: B C
authors.initials: BC
authors.lastname: Lee
authors.forename: I-G
authors.initials: IG
authors.lastname: Choi
authors.forename: D-S
authors.initials: DS
authors.lastname: Kim
authors.forename: T-C
authors.initials: TC
authors.lastname: Kang
mesh_terms: D000818:Animals; D000073883:CX3C Chemokine Receptor 1; D002452:Cell Count / Q000379:methods; D054428:Chemokine CX3CL1 / Q000276:immunology / Q000378:metabolism*; D004195:Disease Models, Animal; D005452:Fluoresceins; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006023:Glycoproteins / Q000378:metabolism; D006624:Hippocampus / Q000187:drug effects / Q000473:pathology; D007074:Immunoglobulin G / Q000008:administration & dosage; D007276:Injections, Intraventricular / Q000379:methods; D037102:Lectins / Q000378:metabolism; D009474:Neurons / Q000187:drug effects / Q000473:pathology*; D009930:Organic Chemicals; D010862:Pilocarpine; D051381:Rats; D017207:Rats, Sprague-Dawley; D019707:Receptors, Chemokine / Q000276:immunology / Q000378:metabolism*; D013226:Status Epilepticus / Q000139:chemically induced* / Q000473:pathology*; D013997:Time Factors; D053675:Versicans
chemical_list: D000073883:CX3C Chemokine Receptor 1; C516305:CX3CR1 protein, rat; D054428:Chemokine CX3CL1; D005452:Fluoresceins; D005904:Glial Fibrillary Acidic Protein; D006023:Glycoproteins; D007074:Immunoglobulin G; D037102:Lectins; D009930:Organic Chemicals; D019707:Receptors, Chemokine; C508324:Vcan protein, rat; C435731:fluoro jade; D010862:Pilocarpine; D053675:Versicans