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.

Functional recovery after facial nerve crush is delayed in severe combined immunodeficient mice.

The goal of the current study was to determine if T and B lymphocytes play a role in functional recovery after peripheral nerve injury. The time course of behavioral recovery following facial nerve crush injury at the stylomastoid foramen was established in scid mice which lack functional T and B cells and reconstituted scid mice as compared to wild-type mice. The average time necessary for recovery of full eye blink reflex and vibrissae movements in wild-type mice was 10.3+/-0.2 and 9.9+/-0.34 days, respectively. In contrast, recovery of full eye blink reflex and vibrissae movements took 14.8+/-0.54 and 12.3+/-0.41 days, respectively, in scid mice. Reconstitution of scid mice with whole splenocytes resulted in functional recovery times similar to wild-type, with eye blink reflex recovery and vibrissae movement being 10.5+/-0.3 and 10.0+/-0.0 days, respectively. These results suggest that the delayed behavioral recovery time observed in scid mice may be due to the absence of T and B lymphocytes.

CD4+ T, but not CD8+ or B, lymphocytes mediate facial motoneuron survival after facial nerve transection.

The capacity of facial motor neurons (FMN) to survive injury and successfully regenerate is substantially compromised in immunodeficient mice, which lack T and B lymphocytes (). The goal of the present study was to determine which T cell subset (CD4+ and/or CD8+), and whether the B lymphocyte, is involved in FMN survival after nerve injury. All mice were subjected to a right facial nerve axotomy, with the left (uncut) side serving as an internal control. FMN survival, of the right (cut) side, was measured 4 weeks post-operative, and expressed as a percentage of the left (uncut) control side. FMN survival in wild-type mice was 86%+/-1.5. In contrast, FMN survival in CD4 KO mice was 60%+/-2.0. Reconstitution of either CD4 KO mice, or recombinase activating gene-2 knockout (RAG-2 KO) mice (which lack functional T and B cells) with CD4+ T cells alone restored FMN survival to wild-type levels (85%+/-1.2 and 84%+/-2.5, respectively). There was no difference in FMN survival between wild-type, CD8 KO and MmuMT (B cell deficient) mice. Reconstitution of RAG-2 KO mice with CD8+ T cells alone, or B cells alone, failed to restore FMN survival levels (65%+/-1.5 and 63%+/-1.0, respectively). It is concluded that, of the population of FMN that do not survive injury, CD4+ T lymphocytes, but not CD8+ T lymphocytes or B cells, mediate FMN survival after peripheral nerve injury.