Respiratory Plasticity Following Spinal Injury: Role of Chloride-Dependent Inhibitory Neurotransmission
Technical Report,30 Sep 2013,29 Sep 2016
University of Wisconsin, Madison Madison United States
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Our fundamental goal was to test the hypothesis that spontaneous and induced plasticity in chloride-dependent synaptic inhibition of phrenic motor neurons contributes to functional recovery from chronic cervical spinal contusion CSC injuries. We performed experiments to determine if CSC and repetitive acute intermittent hypoxia rAIH shift the NKCC1KCC2 balance in phrenic motor neurons, degrading CSC and restoring rAIH chloride-dependent synaptic inhibition, and performed experiments to determine if spinal PKC plays a role in spontaneous recovery of breathing following CSC. Our analyses indicate that CSC increases membrane NKCC1, and decreases the membrane-cytosol KCC2 ratio within phrenic motor neurons, consistent with the interpretation that compensatory shifts in NKCC1KCC2 balance in phrenic motor neurons preserves respiratory function following CSC. rAIH had no apparent effects on either protein, although the timing of rAIH delivery may not have been optimal based on newer information . We obtained conflicting results regarding the role of spinal PKC activity in spontaneous recovery of diaphragm EMG and breathing capacity within the first 3 days following injury histological analysis underway will confirm if variations in the extent of injury are associated with these conflicting results.
- Anatomy and Physiology
- Weapons Effects (Biological)