Literature DB >> 7852624

trk-immunoreactivity in the monkey central nervous system: forebrain.

J H Kordower1, E Y Chen, J R Sladek, E J Mufson.   

Abstract

Neurotrophins such as nerve growth factor (NGF) mediate their effects through interactions with high-affinity tropomycin-related kinase (trk) receptors. The present study employed a polyclonal antibody to characterize the distribution of trk-immunoreactive neurons within the nonhuman primate brain. Both young adult and aged cebus and rhesus monkeys displayed trk-immunoreactive neurons within all subdivisions of the basal forebrain. Colocalization studies revealed that between 66% and 76% of trk-immunoreactive basal forebrain neurons also expressed immunoreactivity for the low-affinity p75 NGF receptor, an excellent marker for cholinergic basal forebrain cells. In this experiment, most single-labeled basal forebrain neurons contained only trk immunoreactivity, whereas 4% of basal forebrain neurons expressed only the low-affinity p75 NGF receptor. Scattered trk-immunoreactive neurons also were observed within the caudate nucleus and putamen. Although dual-localization studies with choline acetyltransferase (ChAT) were not performed, striatal neurons codistributed with ChAT-immunoreactive cells, and both types of cells were similar in size and morphology. This suggests that trk immunoreactivity is expressed within cholinergic interneurons within the primate striatum. Finally, lightly stained trk-immunoreactive neurons were observed within the stratum oriens of the hippocampal formation and within the hypothalamus. These data indicate that both cholinergic and, possibly, noncholinergic forebrain neurons express the protein for the high-affinity trk receptor, which transduces the signal mediating the trophic effects of neurotrophins. In addition, the pattern of trk immunoreactivity was preserved in two aged (26 and 29 years old) rhesus monkeys, suggesting that the expression of trk, for the most part, is sustained throughout the lifetime of the organism.

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Year:  1994        PMID: 7852624     DOI: 10.1002/cne.903490103

Source DB:  PubMed          Journal:  J Comp Neurol        ISSN: 0021-9967            Impact factor:   3.215


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