TESTOSTERONE REGULATION OF THE REGENERATIVE PROPERTIES OF INJURED RAT SCIATIC MOTOR-NEURONS

We have previously demonstrated that systemic administration of testosterone differentially regulates the regenerative properties of injured hamster facial motor neurons, which are androgen receptor-containing cranial motor neurons. In this investigation, the hypothesis that testosterone alters the regenerative properties of rat sciatic motor neurons, which are androgen receptor-containing spinal motor neurons, was tested using fast axonal transport of radioactively labeled proteins to assess sciatic nerve regeneration. Adult castrated male rats were subjected to crush axotomy of the sciatic nerve at the level of the gemelli tendons (mid-thigh). One-half of the axotomized animals received subcutaneous implants of testosterone propionate (TP), with the remainder of the animals sham implanted with blank capsules. The outgrowth distances of the leading axons were measured at 5, 6, 7, and 11 days postoperative. Linear regression analysis was accomplished, with the slope of the line representing the regeneration rate and the x-intercept the initial delay of sprout formation. Systemic administration of testosterone resulted in a 13% increase in the rate of regeneration, relative to the control, -TP group. Outgrowth distances were significantly increased in the + TP group only in the later stages of regeneration. However, TP did not shorten the delay in sprout formation in regenerating sciatic motor neurons, but instead produced a small prolongation in the delay time. This pattern of hormonal regulation of the regenerative properties of spinal motoneurons is similar to that previously found in cranial motoneurons. The prolongation of the initial delay may have been a factor in the lack of significant out-growth distances during the early stages of regeneration. The magnitude of the effects of TP on male rat sciatic motor neurons are less pronounced than in male hamster facial motor neurons, but quite similar to those effects observed in female hamster facial motor neurons. Why this is the case is not known, but may be related to a number of factors discussed in the text.