Trkb receptors modulation of glutamate release is limited to a subset of nerve terminals in the adult rat hippocampus

• Autor(a) principal: Pereira, Daniela B.
• Data de Publicação: 2006
• Outros Autores: Rebola, Nelson, Rodrigues, Ricardo J., Cunha, Rodrigo A., Carvalho, Arsélio P., Duarte, Carlos B.
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Científico de Acesso Aberto de Portugal (Repositórios Cientìficos)
• DOI: 10.1002/jnr.20784
• Texto Completo: http://hdl.handle.net/10316/8320; https://doi.org/10.1002/jnr.20784

Brain-derived neurotrophic factor (BDNF) modulates glutamatergic excitatory transmission in hippocampal primary cultures by acting at a presynaptic locus. Although it has been suggested that BDNF also modulates adult hippocampus glutamatergic transmission, this remains a matter of controversy. To clarify a putative role for this neurotrophin in the modulation of glutamate release we applied exogenous BDNF to isolated adult rat hippocampal nerve terminals. BDNF, at 100 ng/ml, potentiated by 25% the K+-evoked release of [3H]glutamate from hippocampal synaptosomes. The small effect of BDNF on [3H]glutamate release correlated with a modest increase in phospholipase Cgamma (PLCgamma) phosphorylation, and with the lack of effect of BDNF on extracellular-signal regulated kinase (ERK) and Akt phosphorylation. Immunocytochemistry studies demonstrated that only about one-third of glutamatergic synaptosomes were positive for TrkB immunoreactivity. Furthermore, biotinylation and subsynaptic fractionation studies showed that only one-fourth of total full-length TrkB was present at the plasma membrane, evenly distributed between the presynaptic active zone and the postsynaptic density. These results indicate that BDNF modulates synaptic transmission presynaptically in a small subset of hippocampal glutamatergic synapses that contain TrkB and that express the receptor on the plasma membrane. © 2006 Wiley-Liss, Inc.