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Androgen regulates trkB immunolabeling in spinal motoneurons
Author(s) -
Osborne M.C.,
Verhovshek T.,
Sengelaub D.R.
Publication year - 2006
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.21122
Subject(s) - tropomyosin receptor kinase b , testosterone (patch) , androgen receptor , endocrinology , medicine , bulbocavernosus reflex , neurotrophic factors , androgen , receptor , brain derived neurotrophic factor , aromatase , biology , neurotrophin , neuroprotection , neuroscience , hormone , spinal cord , prostate cancer , cancer , breast cancer
Neurotrophic factors and steroid hormones have been shown to have neuroprotective/neurotherapeutic effects, and it has been shown previously that brain‐derived neurotrophic factor (BDNF) and testosterone have a combinatorial effect in the maintenance of motoneurons. Given that gonadal hormones regulate the BDNF receptor, tyrosine receptor kinase B (trkB), we hypothesized that such a regulatory effect could mediate the interactive effects of BDNF and testosterone. Using immunohistochemical methods, we examined the frequency of cells immunolabeled for trkB receptors in two populations of spinal motoneurons, the hormone‐sensitive, sexually dimorphic motoneurons of the spinal nucleus of the bulbocavernosus (SNB) and the nondimorphic motoneurons innervating the muscles of the quadriceps. In both the highly androgen‐sensitive SNB motoneurons and the more typical somatic motoneurons innervating the quadriceps, the frequency of motoneurons intensely immunolabeled for trkB receptors was regulated by the presence of testosterone. Castrated animals deprived of testosterone showed a reduced frequency of intensely labeled motoneurons compared with intact animals or castrated animals given testosterone replacement. This finding suggests that the combinatorial effect of BDNF and testosterone in the maintenance of motoneurons could occur at least in part through an androgen‐mediated expression of the BDNF receptor. © 2006 Wiley‐Liss, Inc.