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

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.

Relationship of Brain-Derived Neurotrophic Factor and Its Receptor TrkB to Altered Inhibitory Prefrontal Circuitry in Schizophrenia

“…Consistent with previous observations in primate association cortices (Okuno et al, 1999;, the hybridization signal for TrkC mRNA was detected in layers II, III, V, and VI, mainly in neurons, in area 9 of control and schizophrenia subjects ( Fig. 1 E, F ).…”

“…The TrkB mRNA was expressed by the majority of neurons across layers II-VI and by a few in layer I (data not shown). These expression patterns in control subjects were consistent with previously published observations in monkey and human association cortices (Okuno et al, 1999;Hashimoto et al, 2000;Romanczyk et al, 2002;Weickert et al, 2003).…”

“…The fragments for TrkB and TrkC mRNAs were amplified from the regions encoding the intracellular domains that are specific to the tyrosine kinase-containing isoforms. Antisense riboprobes transcribed from these fragments were shown to detect the specific signal of targeted mRNAs in the primate neocortex (Okuno et al, 1999;Hashimoto et al, 2000). To increase signal intensity for BDNF mRNA, we amplified an additional 358 bp fragment, corresponding to bases 693-1037 of the BDNF mRNA (GenBank accession number M61181), and combined the two antisense riboprobes transcribed from the two fragments.…”

Spatiotemporal Dynamics of Brain-Derived Neurotrophic Factor mRNA Induction in the Vestibulo-Olivary Network during Vestibular Compensation

“…E xpression levels of mRNAs were quantified by using an RT-PCR coamplification method as described previously (Tokuyama et al, 1998Okuno et al, 1999). Specific primers for PCR coamplification were designed based on the published sequences of rat BDN F (GenBank accession number M61175), trkB (GenBank accession number M55291), c-fos (GenBank accession number X06769), ␣-tubulin (GenBank accession number V10227), and hypoxanthineguanine phosphoribosyltransferase (hprt) (GenBank accession number M63983) genes.…”

“…The procedures of reverse transcription and PCR coamplification were essentially the same as described previously (Tokuyama et al, 1998;Okuno et al, 1999). In the present study, the hprt gene was used as an internal standard gene .…”