title: Expression of Semaphorin3C in axotomized rodent facial and rubrospinal neurons.
abstract: Semaphorins are a family of axonal guidance molecules that, by virtue of their chemorepulsive or chemoattractive actions, may be the important factors in determining the success or failure of axonal regeneration in the mature nervous system after injury. Here, we have used two adult mouse models of nervous system injury to evaluate the neuronal expression of Semaphorin3C (Sema3C) in regenerating (facial motoneurons) and non-regenerating (rubrospinal) neurons following axonal injury. Using in situ hybridization (ISH), we observed that uninjured facial motoneurons express Sema3C mRNA and, following axonal injury, there is a transient up-regulation in Sema3C mRNA expression in injured motoneurons. In contrast, Sema3C mRNA was not detected in uninjured rubrospinal neurons; however, following axotomy, injured rubrospinal neurons significantly up-regulate Sema3C mRNA expression. The increase in Sema3C mRNA expression in axotomized rubrospinal neurons was not limited to the mouse nervous system: serial dilution RT-PCR analysis revealed a similar increase in Sema3C mRNA expression in the axotomized rat rubrospinal nucleus, 3 days following a rubrospinal tract lesion. This demonstrates that increased Sema3C mRNA levels in axotomized rubrospinal neurons is common to both mouse and rat injury models.
authors.affiliation: ICORD (International Collaboration on Repair Discoveries), 6270 University Boulevard, University of British Columbia, Vancouver, BC, Canada V6T 1Z4.
authors.forename: Loren W
authors.initials: LW
authors.lastname: Oschipok
authors.forename: Joshua
authors.initials: J
authors.lastname: Teh
authors.forename: Lowell T
authors.initials: LT
authors.lastname: McPhail
authors.forename: Wolfram
authors.initials: W
authors.lastname: Tetzlaff
mesh_terms: D000818:Animals; D019771:Axotomy; D004195:Disease Models, Animal; D004525:Efferent Pathways / Q000378:metabolism / Q000503:physiopathology; D005154:Facial Nerve / Q000378:metabolism / Q000503:physiopathology; D020220:Facial Nerve Injuries / Q000378:metabolism* / Q000503:physiopathology; D005786:Gene Expression Regulation / Q000502:physiology; D020439:Growth Cones / Q000378:metabolism*; D017403:In Situ Hybridization; D008297:Male; D051379:Mice; D009046:Motor Neurons / Q000378:metabolism; D009416:Nerve Regeneration / Q000502:physiology*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012012:Red Nucleus / Q000378:metabolism / Q000503:physiopathology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012249:Rhombencephalon / Q000378:metabolism / Q000503:physiopathology; D039961:Semaphorins / Q000235:genetics / Q000378:metabolism*; D013116:Spinal Cord / Q000378:metabolism / Q000503:physiopathology; D013119:Spinal Cord Injuries / Q000378:metabolism* / Q000503:physiopathology; D015854:Up-Regulation / Q000502:physiology*
chemical_list: D012333:RNA, Messenger; D039961:Semaphorins; C510203:semaphorin 3C protein, mouse