title: Axotomy transiently down-regulates androgen receptors in motoneurons of the spinal nucleus of the bulbocavernosus.
abstract: Testosterone is an important trophic factor for motoneurons in the spinal nucleus of the bulbocavernosus (SNB), and SNB motoneurons are more responsive to testosterone than are other motoneurons. Axonal injury during early postnatal life prevents the normal development of steroid-sensitivity by adult SNB motoneurons. Axonal injury also causes changes in the expression by motoneurons of a wide range of proteins, including the up-regulation of trophic factor receptors. We have used a polyclonal antibody (PG-21; G.S. Prins) to study the expression of androgen receptors in SNB motoneurons after axonal injury. PG-21 labeled motoneuronal nuclei in the lower lumbar spinal cord of rats in a pattern that matched autoradiographic reports of androgen accumulation in this region of the nervous system. A population of numerous, small cells located dorsal to the central canal also showed evidence of androgen receptor expression. Cutting the axons of SNB motoneurons in adulthood or in development caused a decrease in androgen receptor immunoreactivity in SNB motoneurons. This is the first report that a trophic factor receptor in motoneurons is down-regulated after axonal injury, and is interesting in light of reports that testosterone treatment can facilitate motoneuronal regeneration after nerve cut. Androgen receptor levels subsequently returned to normal, regardless of the age at axotomy, providing no evidence for a lasting effect of developmental axotomy on androgen receptor levels in SNB motoneurons. Thus, axotomy-induced down-regulation of androgen receptors does not underlie the inability of SNB motoneurons to respond to androgen treatment several months after pudendal nerve cut in development.
authors.affiliation: Program in Neuroscience, University of California, Los Angeles 90095-1761, USA.
authors.forename: J L
authors.initials: JL
authors.lastname: Lubischer
authors.forename: A P
authors.initials: AP
authors.lastname: Arnold
mesh_terms: D000375:Aging / Q000378:metabolism; D000818:Animals; D000831:Animals, Newborn / Q000254:growth & development / Q000378:metabolism; D001345:Autoradiography; D001369:Axons / Q000502:physiology*; D003714:Denervation; D015536:Down-Regulation; D007150:Immunohistochemistry; D008297:Male; D009046:Motor Neurons / Q000378:metabolism*; D009424:Nervous System Physiological Phenomena; D010413:Penis / Q000294:innervation*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011944:Receptors, Androgen / Q000378:metabolism*; D013116:Spinal Cord / Q000502:physiology*; D013997:Time Factors
chemical_list: D011944:Receptors, Androgen