Testosterone treatment attenuates the effects of facial nerve transection on glial fibrillary acidic protein (GFAP) levels in the hamster facial motor nucleus.
Testosterone propionate (TP) administration coincident with facial nerve injury accelerates the recovery rate from facial muscle paralysis in the hamster. One mechanism by which TP could augment peripheral nerve regeneration is through glial fibrillary acidic protein (GFAP) regulation in the facial motor nucleus. In a previous study, axotomy alone induces increases in GFAP mRNA. with TP significantly attenuating the axotomy-induced increases in GFAP mRNA. In the present study, immunoblotting techniques were used to extend our previous GFAP mRNA studies to the protein level. Castrated male hamsters were subjected to a right facial nerve transection, with half of the animals receiving subcutaneous implants of 100% crystalline TP. The left facial motor nucleus of each animal served as an internal control. Postoperative survival times include Days 4, 7, and 14. In non-TP-treated animals, facial nerve transections alone increased GFAP levels at all time points, relative to internal controls. As previously observed at the mRNA level, TP treatment attenuated but did not eliminate the axotomy-induced increase in GFAP levels at all time points tested. These results suggest that the regulatory actions of gonadal steroids on GFAP expression manifested in parallel at the mRNA/protein levels.
Coers
Susanna
S
Department of Cell Biology, Neurobiology, and Anatomy, Stritch School of Medicine, Loyola University of Chicago, Maywood, Illinois 60153, USA. scoers@lumc.edu
Tanzer
Lisa
L
Jones
Kathryn J
KJ
D000818:Animals; D001253:Astrocytes / Q000187:drug effects / Q000378:metabolism; D006224:Cricetinae; D005154:Facial Nerve / Q000187:drug effects* / Q000473:pathology / Q000503:physiopathology; D020220:Facial Nerve Injuries / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D015870:Gene Expression / Q000187:drug effects / Q000502:physiology; D005904:Glial Fibrillary Acidic Protein / Q000187:drug effects* / Q000378:metabolism; D005911:Gliosis / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D009046:Motor Neurons / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D018696:Neuroprotective Agents / Q000494:pharmacology*; D012183:Retrograde Degeneration / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D013739:Testosterone / Q000378:metabolism / Q000494:pharmacology*; D015854:Up-Regulation / Q000187:drug effects / Q000502:physiology
D005904:Glial Fibrillary Acidic Protein; D018696:Neuroprotective Agents; D013739:Testosterone