A collection of neurons in the upper lumbar spinal cord of male rats projects to the lower lumbar spinal cord, releasing
gastrin-releasing peptide (GRP) onto somatic and autonomic centers known to regulate male sexual reflexes such as erection and ejaculation. Because these reflexes are
androgen dependent, we asked whether manipulating levels of
androgen in adult rats would affect GRP expression in this spinal center. We found that
castration resulted, 28 d later, in a profound decrease in the expression of GRP in the spinal cord, as reflected in immunocytochemistry and competitive ELISA for the
protein as well as real-time quantitative PCR for the transcript. These effects were prevented if the castrates were treated with
testosterone propionate. Genetically male (XY) rats with the dysfunctional
testicular feminization allele for the
androgen receptor (AR) displayed GRP
mRNA and
protein levels in the spinal cord similar to those of females, indicating that
androgen normally maintains the system through AR. We saw no effect of
castration or the
testicular feminization allele on expression of the receptor for GRP in the spinal cord, but
castration did reduce expression of AR transcripts within the spinal cord as revealed by real-time quantitative PCR and Western blots. Taken together, these results suggest that
androgen signaling plays a pivotal role in the regulation of GRP expression in male lumbar spinal cord. A greater understanding of how
androgen modulates the spinal GRP system might lead to new therapeutic approaches to male sexual dysfunction.