title: IQGAP1 expression in spared CA1 neurons after an excitotoxic lesion in the mouse hippocampus.
abstract: Repeated seizures induce permanent alterations in the hippocampal circuits in experimental models with intractable temporal lobe epilepsy. Sprouting and synaptic reorganization induced by seizures has been well-studied in the mossy fiber pathway. However, studies investigating sprouting and synaptic reorganization beyond the mossy fiber pathway are limited. The present study examined the biochemical changes of CA1 pyramidal neurons undergoing morphological changes after excitotoxicity-induced hippocampal CA3 neuronal death. IQ-domain GTPase-activating proteins (IQGAP1), is an effector of Rac1 and Cdc42 and an actin-binding protein, was upregulated in CA1 pyramidal neurons after kainic acid-induced hippocampal CA3 neuronal degeneration. IQGAP1 + cells were colocalized with Nestin, but not in astrocytes or mature neurons. Furthermore, IQGAP1 did not originate from newly divided local precursors or NG2 + cells. IQGAP1 and adenomatous polyposis coli localized in CA1 pyramidal neurons, and Cdc42 activation was followed by IQGAP1 recruitment. These findings suggest that IQGAP1 is upregulated in pre-existed sparing neurons of the CA1 layer undergoing morphological changes after excitoxicity-induced hippocampal CA3 neuronal death. It demonstrates the utility of IQGAP1 as a possible marker for spared pyramidal neurons, which may contribute to structural and functional alternations responsible for the development of epilepsy.
authors.affiliation: Department of Anatomy, Brain Research Institute, Chungnam National University School of Medicine, Daejeon, 301-747, South Korea.
authors.forename: Min-Hee
authors.initials: MH
authors.lastname: Yi
authors.forename: Sooil
authors.initials: S
authors.lastname: Kim
authors.forename: Enji
authors.initials: E
authors.lastname: Zhang
authors.forename: Joon Won
authors.initials: JW
authors.lastname: Kang
authors.forename: Jin Bong
authors.initials: JB
authors.lastname: Park
authors.forename: Young Ho
authors.initials: YH
authors.lastname: Lee
authors.forename: Chun Kee
authors.initials: CK
authors.lastname: Chung
authors.forename: Yong Min
authors.initials: YM
authors.lastname: Kim
authors.forename: Dong Woon
authors.initials: DW
authors.lastname: Kim
mesh_terms: D025601:Adenomatous Polyposis Coli Protein / Q000378:metabolism; D000818:Animals; D000941:Antigens / Q000378:metabolism; D001253:Astrocytes / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D015415:Biomarkers / Q000378:metabolism; D056547:CA1 Region, Hippocampal / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology*; D002454:Cell Differentiation / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D004268:DNA-Binding Proteins; D005455:Fluorescent Antibody Technique; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D007608:Kainic Acid; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009419:Nerve Tissue Proteins / Q000378:metabolism; D064231:Nestin / Q000378:metabolism; D009457:Neuroglia / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D009474:Neurons / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology*; D009498:Neurotoxins / Q000633:toxicity*; D009687:Nuclear Proteins / Q000378:metabolism; D011509:Proteoglycans / Q000378:metabolism; D055748:SOXB1 Transcription Factors / Q000378:metabolism; D015854:Up-Regulation / Q000187:drug effects; D020703:ras GTPase-Activating Proteins / Q000378:metabolism*; D000099216:Chondroitin Sulfate Proteoglycan 4
chemical_list: D025601:Adenomatous Polyposis Coli Protein; D000941:Antigens; D015415:Biomarkers; D004268:DNA-Binding Proteins; D005904:Glial Fibrillary Acidic Protein; D007608:Kainic Acid; D009419:Nerve Tissue Proteins; D064231:Nestin; D009498:Neurotoxins; D009687:Nuclear Proteins; D011509:Proteoglycans; D055748:SOXB1 Transcription Factors; D020703:ras GTPase-Activating Proteins; D000099216:Chondroitin Sulfate Proteoglycan 4; C101203:IQ motif containing GTPase activating protein 1; C492380:NeuN protein, mouse
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