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Methods for the Modulation and Analysis of NF-κB-dependent Adult Neurogenesis
Published on: February 13, 2014
BDNF and trkB mRNA expression in the hippocampus and temporal cortex during the human lifespan
M J Webster1, M M Herman, J E Kleinman
1Stanley Laboratory of Brain Research, USUHS, Bethesda, MD 20814, USA. websterm@stanleyresearch.org
Abstract:
Brain-derived neurotrophic factor (BDNF) and its receptor tyrosine kinase B (trkB) influence neuronal survival, differentiation, synaptogenesis, and maintenance. Using in situ hybridization we examined the spatial and temporal expression of mRNAs encoding these proteins during diverse stages of life in the human hippocampus and inferior temporal cortex. We examined six postnatal time points: neonatal (1-3 months), infant (4-12 months), adolescent (14-18 years), young adult (20-24 years), adult (34-43 years), and aged (68-86 years). Within the hippocampus, levels of BDNF mRNA did not change significantly with age. However, levels of both the full-length form of trkB (trkB TK+) mRNA and the truncated form of trkB (trkB TK-) decreased over the life span (p < 0.05). In the temporal cortex, BDNF and trkB TK+ mRNA levels were highest in neonates and decreased with age (r = -0.4 and r = -0.7, respectively, both p < 0.05). In contrast, TrkB TK- mRNA levels remained constant across the life span in the temporal cortex. The peak in both BDNF and trkB TK+ mRNA expression in the neonate temporal cortex differs from that previously described for the frontal cortex where both mRNAs peak in expression during young adulthood. The increase in BDNF and trkB TK+ mRNA in the temporal cortex of the neonate suggests that neurotrophin signaling is important in the early development of the temporal cortex. In addition, since BDNF and both forms of its high affinity receptor are expressed throughout the development, maturation, and aging of the human hippocampus and surrounding neocortex they are likely to play roles not only in early growth but also in maintenance of neurons throughout life.
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