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Brain‐Derived Neurotrophic Factor Increases the Stimulation‐Evoked Release of Glutamate and the Levels of Exocytosis‐Associated Proteins in Cultured Cortical Neurons from Embryonic Rats
Author(s) -
Takei Nobuyuki,
Sasaoka Kumi,
Inoue Ko,
Takahashi Masami,
Endo Yasuhisa,
Hatanaka Hiroshi
Publication year - 1997
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1997.68010370.x
Subject(s) - exocytosis , glutamate receptor , neuroscience , neurotrophic factors , stimulation , brain derived neurotrophic factor , embryonic stem cell , neurotrophin , cortical neurons , biology , chemistry , microbiology and biotechnology , endocrinology , biochemistry , receptor , secretion , gene
Differentiation and survival of neurons induced by neurotrophins have been widely investigated, but little has been reported about the long‐term effect of brain‐derived neurotrophic factor (BDNF) on synaptic transmission. Among many steps of neurotransmission, one important step is regulated release of transmitters. Therefore, the release of glutamate and GABA from cortical neurons cultured for several days with or without BDNF was measured by an HPLC‐fluorescence method. Although BDNF had little effect on the basal release of glutamate, high K + ‐evoked release was greatly increased by BDNF. BDNF also tended to increase evoked release of GABA. Recently, several proteins involved in the step of “regulated release” have been identified. Thus, the effect of BDNF on the levels of these proteins was then investigated. Neurons were cultivated with or without BDNF, collected, and electrophoresed for western blotting. BDNF increased levels of synaptotagmin, synaptobrevin, synaptophysin, and rab3A, which were known as vesicle protein. Levels of syntaxin, SNAP‐25, and β‐SNAP were also increased by BDNF. In addition, the numbers of cored and clear vesicles in nerve terminals or varicosities were also increased by BDNF. These results raise the possibility that BDNF increases regulated release of neurotransmitters through the up‐regulation of secretory mechanisms.