Location: Hall F-J Neuroscience 2012, SfN’s 42nd annual meeting, is scheduled for Oct. 13 -17 in New Orleans at the Ernest N. Morial Convention Center.
Presentation time: Sunday, Oct 14, 2012, 1:00 PM – 2:00 PM
Authors: *D. V. GUTIERREZ, W. J. ALILAIN;
NEUROSCIENCE, METROHEALTH MEDICAL CENTER, CLEVELAND, OH
Abstract: Spinal cord injury (SCI) in the high cervical level (C1-C2) disrupts descending bulbospinal fibers originating from medullary respiratory centers that project to the phrenic motor nucleus. Injuries at this level are quite significant and can induce diaphragm paralysis resulting in dependence on mechanical ventilation. In our laboratory, we employ the lateral C2 hemisection model of SCI which causes paralysis of the ipsilateral hemidiaphragm. Other laboratories utilizing this model have shown that injured animals receiving short exposure to intermittent hypoxia (IH) produces an increased respiratory drive which can strengthen and activate spared pathways to the denervated ipsilateral phrenic nucleus. In the present study, we sought to determine if signaling molecules relevant to plasticity and regeneration are affected by this intervention. Of particular significance to this study is the recent finding that exercise after experimental SCI amplifies the expression and protein levels of mTOR while decreasing PTEN. This is important because the PTEN/mTOR pathway has been shown to influence plasticity, protein synthesis, neurite and axonal outgrowth and regeneration. Therefore in this investigation, we hypothesized that IH exposure would contribute to the modulation of both PTEN and mTOR expression after injury. Data obtained from immunohistochemical analysis revealed an upregulation of mTOR expression in the motor neurons of animals receiving 1 hour of IH training for 5 days post-injury. This increased expression was limited to C2 hemisected groups that were exposed to IH and was not evident in naïve or normoxia treated animals. The results obtained thus far suggest that exposure to IH potentially creates an environment in the CNS after SCI which may promote the plasticity of motor neurons and augment the regenerative capacity of injured axons through the upregulation of mTOR.
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