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J Neurosci Res. 2006 Apr;83(5):832-44.

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

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1
Department of Zoology, Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.

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 [(3)H]glutamate from hippocampal synaptosomes. The small effect of BDNF on [(3)H]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.

PMID:
16477614
DOI:
10.1002/jnr.20784
[Indexed for MEDLINE]
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