title: Differential activation of proapoptotic molecules between mouse and rat models of distal motor trigeminal denervation.
abstract: BACKGROUND
  We previously developed a rat trigeminal motor neuron axotomy model involving masseter and temporal muscle resection to study pathological changes of the central nucleus after peripheral nerve injury caused by oral surgery. Because motor neurons are reported to be more vulnerable to axotomy in mice than rats, we compared the degeneration process of the trigeminal motor nucleus in the rat model with a similar mouse model.
  
  
  METHODS
  We removed masseter and temporal muscles of adult mice or rats. Animals were sacrificed at 3, 7, 14, 28, 42, and 56 days post-operation, and the trigeminal motor nuclei were histologically analyzed.
  
  
  RESULTS
  Size reduction, but no neuronal loss, was seen in the trigeminal motor nuclei in both mice and rats. Time-dependent Noxa expression, starting at 1 week post-operation (wpo), was seen in the mouse model. By 8 wpo, mice expressed a higher level of Noxa than rats. Additionally, we noted persistent expression of cleaved caspase-3 in mice but not in rats. Conversely, apoptosis-inducing factor (AIF), which executes DNA fragmentation in the nucleus, was not translocated to the nucleus in either model.
  
  
  CONCLUSIONS
  Our findings indicate differential activation of motor neuron apoptosis pathways after axotomy in mice and rats. Lack of activation of caspase-independent pathways and distal end denervation in our model might be related to the survival of motor neurons after axonal injury. These findings could be relevant to future neuroprotective strategies for peripheral nerve injury caused by oral surgeries.
authors.affiliation: Department of Neuropathology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
authors.forename: Shiori
authors.initials: S
authors.lastname: Harada
authors.forename: Satoshi O
authors.initials: SO
authors.lastname: Suzuki
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Seki
authors.forename: Seiji
authors.initials: S
authors.lastname: Nakamura
authors.forename: Toru
authors.initials: T
authors.lastname: Iwaki
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D051033:Apoptosis Inducing Factor / Q000032:analysis; D019771:Axotomy; D053148:Caspase 3 / Q000032:analysis; D004195:Disease Models, Animal; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis; D008406:Masseter Muscle / Q000294:innervation; D051379:Mice; D008810:Mice, Inbred C57BL; D008815:Mice, Inbred Strains; D009046:Motor Neurons / Q000473:pathology*; D009410:Nerve Degeneration / Q000473:pathology*; D009434:Neural Pathways / Q000473:pathology; D016501:Neurites / Q000473:pathology; D009457:Neuroglia / Q000473:pathology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D013569:Synapses / Q000473:pathology; D013703:Temporal Muscle / Q000294:innervation; D061221:Trigeminal Nerve Injuries / Q000473:pathology*; D014278:Trigeminal Nuclei / Q000473:pathology*
chemical_list: C494831:Aifm1 protein, rat; D051033:Apoptosis Inducing Factor; D005904:Glial Fibrillary Acidic Protein; C494830:AIFM1 protein, mouse; C408009:Pmaip1 protein, mouse; C539472:Pmaip1 protein, rat; D019253:Proto-Oncogene Proteins c-bcl-2; C505409:Casp3 protein, mouse; C505410:Casp3 protein, rat; D053148:Caspase 3