title: Enhanced GAP-43 gene expression in cortical dysplasia.
abstract: Growth-associated protein GAP-43, a phosphoprotein enriched at presynaptic nerve terminals, is thought to be involved in axonal outgrowth and plasticity in synaptic connections. To explore the synaptic remodeling under the epileptic conditions, we examined GAP-43 expression in brain specimens surgically resected as epileptogenic foci from 17 patients with cortical dysplasia. In situ hybridization with GAP-43 antisense riboprobe showed significantly increased signals in the dysplastic large neurons of cortical dysplasia. Specific distribution with increased immunoreactivity for GAP-43 was not shown in the dysplastic cortex. These results suggest that GAP-43 gene expression is over-expressed in the dysplastic large neurons, reflecting activated synaptic remodeling in the epileptic condition of cortical dysplasia, although the precise site of accelerated synaptic rearrangement remains unknown.
authors.affiliation: Department of Pathology, Gunma University School of Medicine, Maebashi, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Yamanouchi
authors.forename: M
authors.initials: M
authors.lastname: Mizuguchi
authors.forename: A
authors.initials: A
authors.lastname: Oka
authors.forename: S
authors.initials: S
authors.lastname: Takashima
authors.forename: L E
authors.initials: LE
authors.lastname: Becker
authors.forename: M
authors.initials: M
authors.lastname: Eguchi
authors.forename: Y
authors.initials: Y
authors.lastname: Nakazato
mesh_terms: D002540:Cerebral Cortex / Q000002:abnormalities* / Q000473:pathology / Q000503:physiopathology*; D002648:Child; D002675:Child, Preschool; D000013:Congenital Abnormalities / Q000235:genetics; D004827:Epilepsy / Q000209:etiology; D005260:Female; D019922:GAP-43 Protein / Q000235:genetics* / Q000378:metabolism; D015870:Gene Expression; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D008297:Male
chemical_list: D019922:GAP-43 Protein