Expression of brain-derived neurotrophic factor and tyrosine kinase B receptor proteins in glioneuronal tumors from patients with intractable epilepsy: colocalization with N-methyl-D-aspartic acid receptor.
Acta Neuropathol
; 101(4): 383-92, 2001 Apr.
Article
en En
| MEDLINE
| ID: mdl-11355310
Recent evidence suggests that brain-derived neurotrophic factor (BDNF) and its tyrosine kinase B (TrkB) receptor, in addition to promoting neuronal survival and differentiation, modulates synaptic transmission by increasing N-methyl-D-aspartic acid receptor (NMDAR) activity. Overexpression of BDNF may, then, interfere with normal brain function, causing increased excitability. We have examined the immunohistochemical expression of BDNF, full-length TrkB receptor and the NMDAR subunit 1 and subunit 2A/B proteins (NMDAR1 and NMDAR2A/B) in glioneuronal tumors (gangliogliomas, GG, n = 40; dysembryoplastic neuroepithelial tumors, DNT, n = 15), from patients with chronic intractable epilepsy. The great majority of tumors studied were positive for all markers examined, supporting the high level of neurochemical differentiation of these lesions. BDNF and TrkB immunoreactivity (ir) was mainly observed in the neuronal component of the tumors. In GG, more than 90% of tumors contained very intense BDNF-ir ganglion cells. Double labeling confirmed the presence of BDNF-ir and TrkB-ir in neurons which contained NMDAR1. NMDAR2A/B intensely labeled abnormal neurons in both GG and DNT and co-localized with NMDAR1. The presence of BDNF and its receptor in the neuronal component of GG and DNT may suggest a role for this neurotrophin in the development of these lesions, preventing the death of abnormal neuronal cells. In addition, since these neurons contain both NMDAR1 and NMDAR2A/B subunits, the BDNF-TrkB pathway may also contribute through a modulation of glutamatergic transmission to the intrinsic epileptogenicity of glioneuronal tumors.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Teratoma
/
Neoplasias Encefálicas
/
Regulación Neoplásica de la Expresión Génica
/
Receptores de N-Metil-D-Aspartato
/
Ganglioglioma
/
Factor Neurotrófico Derivado del Encéfalo
/
Receptor trkB
/
Epilepsia
/
Proteínas de Neoplasias
/
Proteínas del Tejido Nervioso
Tipo de estudio:
Etiology_studies
Límite:
Adolescent
/
Adult
/
Child
/
Female
/
Humans
/
Male
Idioma:
En
Revista:
Acta Neuropathol
Año:
2001
Tipo del documento:
Article
País de afiliación:
Países Bajos
Pais de publicación:
Alemania