Neurotrophin Receptor Immunoreactivity in Severe Cerebral Cortical Dysplasia
Article first published online: 24 JUL 2002
Volume 43, Issue Supplement s5, pages 220–226, June 2002
How to Cite
Kim, J.-Y., Roh, J.-K., Lee, S. and Chung, C.-K. (2002), Neurotrophin Receptor Immunoreactivity in Severe Cerebral Cortical Dysplasia. Epilepsia, 43: 220–226. doi: 10.1046/j.1528-1157.43.s.5.33.x
- Issue published online: 24 JUL 2002
- Article first published online: 24 JUL 2002
- Cortical dysplasia;
- Cytomegalic neuron;
- Neurotrophin 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.