Effect of androgen on the expression of gap junction and beta-actin mRNAs in adult rat motoneurons.

Expression of gap junction and beta-actin mRNAs was examined in androgen-sensitive motoneurons of the spinal nucleus of the bulbocavernosus (SNB) in adult male rats by in situ hybridization histochemistry using complementary DNAs encoding rat liver gap junction protein (connexin 32) and chick beta-actin. Hybridizable gap junction and beta-actin mRNAs were localised on the somata and proximal dendrites of SNB motoneurons. Removal of androgen by castration significantly reduced the expression levels of both gap junction and beta-actin mRNAs in the SNB motoneurons, whereas these changes were prevented by testosterone treatment. On the contrary, castration or testosterone treatment did not induce any changes in the expression levels of gap junction and beta-actin mRNAs in the motoneurons of the retrodorsolateral nucleus (RDLN), which accumulate androgen less frequently and sparsely than those in the SNB. These results suggest that androgen regulates the expression of both gap junction and beta-actin genes in the SNB motoneurons and may provide evidence for the molecular mechanisms of hormonally induced neuronal plasticity in the SNB motoneurons.