Premium
Characterization of motoneurons and neuropil using facial nerve axotomy in SOD1 mice
Author(s) -
Haulcomb Melissa M,
Mesnard Nichole A,
Sanders Virginia M,
Jones Kathryn J
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.834.4
Subject(s) - axotomy , neuropil , pathology , facial nerve , sod1 , microglia , medicine , immunocytochemistry , biology , amyotrophic lateral sclerosis , anatomy , central nervous system , inflammation , disease
The facial nerve axotomy is used to study motoneuron (MN) survival and peripheral nerve regeneration. Using this model in wild‐type (WT) mice we have identified two populations of MN, regenerative MN in the ventromedial (VM) subnucleus and degenerative MN in the ventrolateral (VL) subnucleus. Amyotrophic lateral sclerosis (ALS) is a progressive and fatal neurodegenerative disease caused by MN cell death. In the SOD1 transgenic mouse model of ALS, a recent study demonstrated the development of MN populations, one compensatory and one degenerative, following disease progression. To further examine these findings we propose to use facial nerve axotomy as a tool to characterize pre‐symptomatic SOD1 MN or neuropil compared to WT. RT‐PCR was conducted using laser microdissected control vs. axotomized facial nuclei and VM vs. VL subnuclei to determine axotomy‐induced mRNA expression changes in apoptotic‐related genes. We found axotomy‐induced expression of tumor necrosis factor‐á (TNFá) and upregulation of caspase 8 in WT mice. However, SOD1 mice have TNFá constitutively expressed in the facial nucleus, with axotomy‐induced upregulation of both TNFá and caspase 8. The colocalization of TNFá, caspase 8, caspase 3, or TNFR1, with microglia, astrocytes, or MN will be examined via immunocytochemistry. Supported by the Les Turner ALS Foundation (NAM & KJJ) and by NIH grant NS40433 (KJJ & VMS). Grant Funding Source Les Turner ALS Foundation and NIH