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Journal of Neuroscience, Vol 14, 1688-1700, Copyright © 1994 by Society for Neuroscience
Regulation of brain-derived neurotrophic factor (BDNF) expression and release from hippocampal neurons is mediated by non-NMDA type glutamate receptors
C Wetmore, L Olson and AJ Bean
Department of Histology and Neurobiology, Karolinska Institute, Stockholm, Sweden.
We have examined the influence of glutamate on cortical brain-derived
neurotrophic factor (BDNF) expression using in situ hybridization and
immunohistochemistry. Kainic acid (KA) produced an upregulation of
hippocampal and neocortical BDNF mRNA as well as BDNF protein that was
blocked by a non-NMDA antagonist, 6,7-dinitroquinoxaline-2,3-dione (DNQX),
but was not affected by the NMDA antagonist 2-amino-7- phosphonoheptanoic
acid (AP7). Basal levels of BDNF mRNA were not affected by NMDA, DNQX, or
AP7 treatment. BDNF protein was also increased after kainate exposure with
a spatial and temporal course distinct from that seen for the expression of
BDNF mRNA. A dramatic shift in BDNF immunoreactivity (-IR) was observed
from intracellular compartments to the neuropil surrounding CA3 pyramidal
cells 2-3 hr after KA exposure. This shift in localization of BDNF-IR
suggests a constitutive release of BDNF at the level of the cell body and
dendrites. Moreover, we have localized mRNAs for full-length and truncated
trkB, to a co-incident population of neurons and glia. These data suggest
the neurons that produce BDNF also express components necessary for a
biological response to the same neurotrophic factor. The present study also
demonstrates increased BDNF-IR in the mossy fiber terminal zone of
hippocampus after exposure to KA, as well as an increase in trkB mRNA, and
provides evidence of local release of this neurotrophin into the
surrounding neuropil where it would be available for local utilization. The
synthesis and putative release of BDNF from somatic and/or dendritic sites
within the hippocampus provide evidence of a potential autocrine or
paracrine role for BDNF, and establish a local source of trophic support
for the maintenance of synaptic plasticity and anatomic reorganization in
the mature nervous system.
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