Glial fibrillary acidic protein expression in the hamster red nucleus: effects of axotomy and testosterone treatment

Testosterone propionate (TP) administration coincident with facial nerve axotomy in the hamster attenuates glial fibrillary acidic protein (GFAP) expression in the facial nucleus that is normally increased following axotomy alone. This ability of TP to modulate astrocyte activity has been linked to the ability of steroid hormones to enhance the regenerative response of injured motor neurons. In an ongoing study designed to examine the potential influences of steroid hormones on centrally projecting motoneurons, the astrocyte reaction in the red nucleus was examined. In the present study, in situ hybridization was used to assess changes in GFAP mRNA in the hamster red nucleus following spinal cord injury (SCI) and TP treatment. Castrated male hamsters were subjected to right rubrospinal tract (RST) transection at spinal cord level T I, with half the animals implanted subcutaneously with Silastic capsules containing 100% crystalline TP and the remainder sham implanted. The uninjured red nucleus served as an internal control. Postoperative survival times were 1, 2, 7. and 14 days. Qualitative-quantitative analyses of emulsion autoradiograms were accomplished. Axotomy alone resulted in a significant but transient increase in GFAP mRNA levels at 2 days postoperative in the injured red nucleus compared with the contralateral uninjured red nucleus. However, in TP-treated animals, GFAP mRNA levels were no different than control levels at 2 dpo but were significantly increased at 7 dpo relative to contralateral control. Additionally, the increase in GFAP mRNA levels following TP treatment was significantly smaller than following axotomy alone. These data suggest that testosterone both delays and reduces the astrocytic reaction in the red nucleus following rubrospinal tract axotomy, and confirms a difference between peripheral and central glial responses to axotomy and steroid administration. (C) 2003 Elsevier Inc. All rights reserved.