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Maintenance of the spinal nucleus of the bulbocavernosus neuromuscular system is not influenced by physiological levels of glucocorticoids
Author(s) -
Niel Lee,
Alves Philip A.,
Pinzon Natalia,
Holmes Melissa M.,
Lovern Matthew B.,
Monks D. Ashley
Publication year - 2012
Publication title -
developmental neurobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.716
H-Index - 129
eISSN - 1932-846X
pISSN - 1932-8451
DOI - 10.1002/dneu.20883
Subject(s) - bulbocavernosus reflex , biology , medicine , endocrinology , basal (medicine) , glucocorticoid , antiglucocorticoid , endogeny , corticosterone , adrenalectomy , atg12 , central nervous system , neuroscience , glucocorticoid receptor , hormone , spinal cord , autophagy , apoptosis , biochemistry , atg5 , insulin
The spinal nucleus of the bulbocavernosus (SNB) neuromuscular system mediates sexual reflexes, and is highly sexually dimorphic in rats. While maintenance of this system in adulthood is mainly dependent on androgens, there is also evidence to suggest that glucocorticoids may have a catabolic effect. We conducted a series of studies to fully examine the influence of basal glucocorticoids on the size of the SNB motoneurons and the associated bulbocavernosus (BC) and levator ani (LA) muscles. Specifically, we examined whether the muscles and motoneurons of the SNB neuromuscular system are affected by: (1) blockade of endogenous glucocorticoids via delivery of the antagonist RU‐486 at doses ranging from low to high, (2) removal of endogenous glucocorticoids via adrenalectomy, or (3) restoration of physiological corticosterone levels via implants following adrenalectomy. In each study, we found that muscle and motoneuron size were unaffected by glucocorticoid manipulation. In contrast to previous results with supraphysiological levels of glucocorticoids, our results indicate that basal, nonstress levels of glucocorticoids do not influence the size of the BC/LA muscles or their associated SNB motoneurons. © 2011 Wiley Periodicals, Inc. Develop Neurobiol, 2012