Testosterone effects on ribosomal RNA levels in injured peripheral motor neurons: A preliminary report

Abstract

We have previously demonstrated that administration of testosterone to hamsters during the early phases of axonal regeneration following facial nerve injury accelerates both the rate of regeneration of the fastest growing population of axons and the return of functional movement. We hypothesized from those studies that testosterone primes the neuronal cell body in such a way as to accelerate the "switch" from a normal to a reparative state. That hypothesis was tested in this study using ribosomal DNA (rDNA) probes in conjunction with in situ hybridization to map the molecular response of the polymerase I system to axotomy, with and without hormone exposure. Adult male hamsters were subjected to right facial nerve severance, with the left side serving as an internal control. Half the animals were administered testosterone propionate via subcutaneous implants. In situ hybridization using a genomic rDNA probe complementary to the 28S rRNA species was accomplished, and levels of rRNA in injured facial neurons assessed both qualitatively and quantitatively. Our initial findings indicate that testosterone markedly upregulates rRNA levels after injury, and support the hypothesis of an acceleration in the metabolic switch to a reparative state. This leads us, in turn, to suggest that this effect of testosterone on the ribosomal system is causally related to the increase in axonal regeneration rate and return of functional movement previously documented in this system.