Steroid receptor coactivator-1 is not required for androgen-mediated sexual differentiation of spinal motoneurons

Neuroendocrinology. 2003 Jul;78(1):45-51. doi: 10.1159/000071705.


Steroid receptor coactivator-1 (SRC-1) amplifies genomic steroid hormone signal transduction and has been implicated in steroid-mediated sexual differentiation of the mammalian nervous system. We investigated the possible effect of an SRC-1 null mutation on 2 morphological endpoints of androgenic signaling: the number and size of motoneurons within the spinal nucleus of the bulbocavernosus (SNB). In wild-type C57/BL6 mice, SRC-1 immunoreactive nuclei were observed within the SNB and one of its target muscles, the levator ani. However, SRC-1 null mice were indistinguishable from sex-matched wild-type littermates in both SNB number and cross-sectional area of SNB motoneurons. Similarly, we found no difference between SRC-1 null and wildtype littermates in the number or size of motoneurons in the retrodorsolateral nucleus, a motor pool that is not typically sexually differentiated in either number or size. These results demonstrate that SRC-1 is not essential for the development and maintenance of a sexually dimorphic neuromuscular system.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Androgens / physiology*
  • Animals
  • Histone Acetyltransferases
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Motor Neurons / metabolism*
  • Muscle, Skeletal / innervation
  • Nuclear Receptor Coactivator 1
  • Receptors, Steroid / metabolism*
  • Sex Differentiation*
  • Spinal Cord / cytology
  • Spinal Cord / metabolism*
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*


  • Androgens
  • Receptors, Steroid
  • Transcription Factors
  • Histone Acetyltransferases
  • Ncoa1 protein, mouse
  • Nuclear Receptor Coactivator 1