Ontogeny of steroid accumulation in spinal lumbar motoneurons of the rat: implications for androgen's site of action during synapse elimination

CL Jordan, SM Breedlove… - Journal of Comparative …, 1991 - Wiley Online Library
Journal of Comparative Neurology, 1991Wiley Online Library
Androgens influence the postnatal development of motoneurons in the spinal nucleus ofthe
bulbocavernosus (SNB) by regulating neuromuscular synapse elimination, the process
through which multiple axonal inputs are retracted from each muscle fiber until single
innervation is established. In the rat levator ani (LA), one of the target muscles for SNB
motoneurons, much of this loss of multiple innervation can be prevented by prepubertal
androgen treatment. We used steroid autoradiography to measure the ontogeny of steroid …
Abstract
Androgens influence the postnatal development of motoneurons in the spinal nucleus ofthe bulbocavernosus (SNB) by regulating neuromuscular synapse elimination, the process through which multiple axonal inputs are retracted from each muscle fiber until single innervation is established. In the rat levator ani (LA), one of the target muscles for SNB motoneurons, much of this loss of multiple innervation can be prevented by prepubertal androgen treatment. We used steroid autoradiography to measure the ontogeny of steroid accumulation in the SNB and the retrodorsolateral nucleus (RDLN), two motoneuronal groups thought to differ in their sensitivity to androgens. Spinal cord tissue was analyzed from castrated male rats at 7, 14,21, and 60 days of age after injection of radiolabelled testosterone. SNB and RDLN motoneurons differ in the ontogeny of androgen accumulation. Over 80% of SNB motoneurons develop the capacity to accumulate androgen during the second week after birth, during the period when androgen regulates synapse elimination in the LA. In contrast, androgen accumulation in RDLN motoneurons develops much later (after 21 days). These data suggest that androgen may act directly on SNB motoneurons to influence synapse elimination.
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