Affiliations: Research and Development Service, Hines VA Hospital,
P.0. Box 20, Hines, IL 60141, USA | Department of Cell Biology Neurobiology and Anatomy,
Loyola University Chicago, Maywood, IL 60153, USA | Department of Cell Biology and Anatomy, The Chicago
Medical School, North Chicago, IL 60064, USA
Note: [] Corresponding author: Todd J. Brown, Ph.D., Research Service,
Edward Hines, Jr. VA Hospital, Bldg. 1 (1 5 l); Hines, Illinois 6014 1, USA.
Tel.: + 1 708 202 5999; Fax: +1 708 202 2327; E-mail:
brown@rescarch.hines.med.va.gov
Abstract: Purpose: We have previously demonstrated that systemic
administration of testosterone propionate (TP) can accelerate the functional
recovery from hind limb paralysis following sciatic nerve injury in the rat. In
this study, we looked at the molecular mechanisms underlying this phenomenon.
Methods: Castrated adult male rats received a right side sciatic nerve crush at
the level of the sciatic notch, with the left side serving as control. Half the
animals received a subcutaneous implant of TP, the others were sham implanted.
Animals were sacrificed at 1, 3, 7 and 10 days post-operative. Lumbar spinal
cord tissue was harvested and in situ hybridization was performed using a
cytoskeletal cDNA probe complementary to βII-tubulin. Results: On the
injured side, sciatic motoneuron tubulin mRNA levels were increased in alt
groups at alt time points. At 3 and 7 days post- op, the TP treated group had
significantly higher levels of tubulin mRNA. Conclusions: These results suggest
that testosterone enhances the rate of regeneration by increasing the neuronal
cytoskeletal response after axonal injury. Further, these results, coupled with
the results from previous experiments in other rodent models, suggest a common
mechanism for gonadal steroid action on regenerating motoneurons across
species.
