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Journal of Neuroscience, Vol 13, 4001-4014, Copyright © 1993 by Society for Neuroscience
Induction of noncatalytic TrkB neurotrophin receptors during axonal sprouting in the adult hippocampus
KD Beck, F Lamballe, R Klein, M Barbacid, PE Schauwecker, TH McNeill, CE Finch, F Hefti and JR Day
Division of Neurogerontology, Andrus Gerontology Center, University of Southern California, Los Angeles 90089-0191.
Brain-derived neurotrophic factor (BDNF) and its signal transducing
receptor, the TrkB tyrosine protein kinase, are expressed at high levels in
the hippocampus of the adult brain, suggesting a role for BDNF mechanisms
in neuronal plasticity. To test this hypothesis, we used defined lesions of
perforant path and fimbria-fornix, two major hippocampal afferents, to
remove synapses on dendrites of dentate gyrus granule cells and pyramidal
cells of Ammon's horn and induce synaptic rearrangements. These combined
lesions remove afferent connections from entorhinal cortex and septum and
produce massive sprouting of axons of the commissural/associational
pathways into the molecular layer of the hippocampal dentate gyrus. At days
1, 3, and 6, the lesions decreased BDNF mRNA expression ipsilaterally to
approximately 50% of control, with complete recovery at 14 d. The lesions
did not alter trkB mRNA levels in neuronal layers of the hippocampus;
however, they resulted in a pronounced induction of trkB mRNA expression in
hippocampal non- neuronal cells 6-14 d after lesioning. The induction
corresponded in time and place to the synaptic reorganization in the
lesioned hippocampus. The mRNA species newly induced by the lesions
corresponded to those transcripts encoding the noncatalytic TrkB receptor
isoform that lacks the cytoplasmic protein kinase domain. Expression of
mRNAs coding for neurotrophin-3 and the TrkC tyrosine protein kinase were
not altered by the lesions. The findings suggest that truncated
noncatalytic TrkB molecules expressed on the surface of glial cells play an
important role in plasticity of the adult brain, possibly regulating the
concentration of bioactive neurotrophins or the responsiveness of
neurotrophin receptors. Alternatively, they may play a role in presenting
neurotrophin molecules to growing axons.
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