Exogenous testosterone reverses age-related atrophy in a spinal neuromuscular system.
Aging is associated with a variety of pathologies, including motor dysfunctions and reductions in sexual behavior. In male rats, declines in sexual behavior during the aging process may be caused in part by the loss of the lumbar spinal cord motoneurons that innervate the penile musculature. Alternatively, declining sexual behavior may be caused by the precipitous reductions in circulating testosterone that occur during aging. In this paper, we report two experiments examining these issues. In Experiment 1, we counted motoneurons in the lumbar motor nuclei and measured several androgen-sensitive morphological properties of the penile muscles and their innervating motoneurons at several time points during the aging process. Motoneuron number in the lumbar nuclei did not change over time, even with very advanced age. In contrast, the penile muscles and their innervating motoneurons underwent profound atrophy, with muscle weight and motoneuron dendritic length declining to less than 50% of young adult levels. In Experiment 2, we treated aged animals with exogenous testosterone, and then examined their penile neuromuscular systems for morphological changes. Testosterone treatment, both acute and chronic, completely reversed age-related declines in the weight of the penile muscles and in the soma size and dendritic length of their innervating motoneurons. Together, these data suggest that reductions in male sexual behavior during the aging process are caused primarily by declines in testosterone levels rather than motoneuron loss. Furthermore, they raise the possibility that testosterone treatment could play an important role in maintaining neuronal connectivity in the aging body.