Neurotrophin receptor immunoreactivity in severe cerebral cortical dysplasia.
OBJECTIVE
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.
Department of Neurosurgery, College of Medicine, Seoul National University Hospital, Yeunkeun-dong 29, Chongno-ku, Seoul 110-744, Korea.
Joo-Yong
JY
Kim
Jae-Kyu
JK
Roh
Sang Kun
SK
Lee
Chun-Kee
CK
Chung
D000293:Adolescent; D000328:Adult; D001927:Brain Diseases / Q000378:metabolism*; D002540:Cerebral Cortex / Q000378:metabolism*; D002648:Child; D005260:Female; D006801:Humans; D008297:Male; D020800:Receptor, Nerve Growth Factor / Q000378:metabolism; D020813:Receptor, trkB / Q000378:metabolism; D020812:Receptor, trkC / Q000378:metabolism; D017475:Receptors, Nerve Growth Factor / Q000378:metabolism*
D020800:Receptor, Nerve Growth Factor; D017475:Receptors, Nerve Growth Factor; D020813:Receptor, trkB; D020812:Receptor, trkC