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Pro‐survival and pro‐apoptotic factors following axotomy in a murine model of Amyotrophic Lateral Sclerosis.
Author(s) -
Haulcomb Melissa M,
Mesnard Nichole A,
Politis Christine M,
Sanders Virgina M,
Jones Kathryn J
Publication year - 2010
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.24.1_supplement.300.6
Subject(s) - axotomy , amyotrophic lateral sclerosis , sod1 , cx3cr1 , medicine , apoptosis , facial nerve , pathology , biology , neuroscience , microbiology and biotechnology , regeneration (biology) , inflammation , disease , chemokine , biochemistry , chemokine receptor
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 neurodegenerative disease caused by MN cell death. In the SOD1 mouse model of ALS, a recent study demonstrated the development of two 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 response compared to WT. We hypothesize that the axotomy‐induced facial motoneuron loss in SOD1 relative to WT, is due to a pro‐inflammatory microenvironment resulting in apoptosis. 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 pro‐apoptotic genes (FasR, Caspase‐3, TNFR1) and pro‐survival genes (PAC1‐R, TNFR2, CX3CR1). Localization of TNFR1, TNFR2, and CX3CR1 will also be examined via immunohistoochemistry. Grant Funding Source: NIH grant NS40433