Fig 7.

17-AAG and rapamycin treatments do not enhance facial motor neuron survival following injury. (A) Histogram of stereological counts of facial motor neurons from mice treated with 17-AAG (10 mg/kg) or vehicle performed at 4 days after axotomy. Similar to rapamycin, treatment with 17-AAG did not enhance levels of motor neuron survival compared to controls (22 ± 1% versus 25 ± 2% for 17-AAG and vehicle-treated groups, respectively), indicating these respective immunophilin-related pathways are not involved in neuroprotection. (B) depicts a typical injured facial nucleus from an animal treated daily with 17-AAG following axotomy. (C) Histogram of facial motor neuron survival following rapamycin treatment. Mice receiving daily rapamycin administration (3 mg/kg) following injury until time of killing showed no significant difference in motor neuron survival compared to vehicle-treated controls (17 ± 2% versus 13 ± 1%, respectively). Shown in (D) is a typical injured facial nucleus from rapamycin-treated animals.