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Neurotrophin Receptor Immunoreactivity in Severe Cerebral Cortical Dysplasia
Author(s) -
Kim JooYong,
Roh JaeKyu,
Lee Sang Kun,
Chung ChunKee
Publication year - 2002
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1046/j.1528-1157.43.s.5.33.x
Subject(s) - tropomyosin receptor kinase b , tropomyosin receptor kinase c , neurotrophin , cortical dysplasia , tropomyosin receptor kinase a , neuroscience , biology , low affinity nerve growth factor receptor , brain derived neurotrophic factor , synaptophysin , neurotrophic factors , pathology , neurotrophin 3 , cerebral cortex , immunohistochemistry , medicine , receptor , epilepsy , growth factor , biochemistry , platelet derived growth factor receptor
Summary: Purpose: Cerebral cortical dysplasia (CD) is one of the important causes of intractable epilepsies and characterized histologically by disorganized cortical lamination and cytomegalic dysplastic neurons. Although it has been suggested that neurotrophins play an important role in differentiation, growth, and survival of developmental neurons, their pathogenetic role in CD has rarely been investigated. Methods: To know the pathogenetic role of various neurotrophins on dysplastic neurons, immunohistochemical staining was performed using antibodies against NGFRp75, trkA, trkB, and trkC in surgical specimens of 20 patients with CD. Results: TrkB and trkC were strongly expressed in dysplastic neurons of severe CD, and NGFRp75 was also expressed in some dysplastic neurons. Conclusions: It is known that brain‐derived neurotrophic factor (BDNF) and neurotrophin‐3 (NT‐3) contribute to the differentiation of neuronal precursor cells, dendritic and axonal arborization, synaptic plasticity, and cellular hyperexcitability, so increased expression of trkB and trkC may have a critical pathogenetic role in cytoskeletal abnormalities and epileptogenicity in dysplastic neurons of CD.