Quantitative evaluation of neurotrophin andtrk mRNA expression in visual and limbic areas along the occipito-temporo-hippocampal pathway in adult macaque monkeys

ArticleinThe Journal of Comparative Neurology 408(3):378-98 · July 1999with2 Reads
Impact Factor: 3.23 · DOI: 10.1002/(SICI)1096-9861(19990607)408:33.0.CO;2-A · Source: PubMed

    Abstract

    The neurotrophins have been implicated in shaping and remodeling the connectivity of neural circuits. To explore the role of neurotrophins and their receptors, Trks, in cortical neural circuits of adult macaque monkeys, we determined mRNA expression levels of neurotrophins and Trk receptors in various visual and limbic areas along the occipito-temporo-hippocampal pathway by using a quantitative reverse-transcription polymerase chain reaction technique. The expression level of brain-derived neurotrophic factor (BDNF) mRNA was lowest in the primary visual cortex (V1), moderate in the temporal visual association area, and highest in the hippocampus. The expression levels of trkB mRNA isoforms, the full-length form that encodes a receptor tyrosine kinase and the truncated form that encodes a noncatalytic receptor, were also low in V1, moderate in the visual association area, and high in the entorhinal cortex. However, in contrast to their ligand BDNF, the expression levels of both trkB isoforms in the hippocampus were significantly lower than those in the entorhinal cortex. NT-3 mRNA was detectable only in the hippocampus and the entorhinal cortex, whereas both the full-length and the truncated forms of trkC mRNA were widely distributed throughout the neocortex and the limbic cortex. The expression levels of NGF and trkA mRNAs in these cortical areas were too low to determine quantitatively. The present findings suggest that, among neurotrophin/Trk signaling systems, the BDNF/TrkB-mediated signal most likely contributes to stabilization, remodeling, or both, of neural circuits in cortical areas along the occipito-temporo-hippocampal pathway in the adult macaque monkey.