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|Title:||Trkb receptors modulation of glutamate release is limited to a subset of nerve terminals in the adult rat hippocampus||Authors:||Pereira, Daniela B.
Rodrigues, Ricardo J.
Cunha, Rodrigo A.
Carvalho, Arsélio P.
Duarte, Carlos B.
|Issue Date:||2006||Citation:||Journal of Neuroscience Research. 83:5 (2006) 832-844||Abstract:||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.||URI:||http://hdl.handle.net/10316/8320||DOI:||10.1002/jnr.20784||Rights:||openAccess|
|Appears in Collections:||FCTUC Ciências da Vida - Artigos em Revistas Internacionais|
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