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. Author manuscript; available in PMC: 2015 Jun 1.
Published in final edited form as: Exp Neurol. 2014 Mar 25;256:46–56. doi: 10.1016/j.expneurol.2014.03.007

Figure 2.

Figure 2

Unilateral reduction in phrenic synaptic inputs at C2 elicits ipsilateral iPMF and csPMF. A, Representative compressed ipsilateral (top) and contralateral (bottom) phrenic neurograms during baseline, ~30 min of unilateral C2 axon conduction block (left), or control injection (right) and 60 min following axon conduction recovery or equivalent duration after control injection “time controls”. Black arrows denote intraspinal injections. Average change in B, ipsilateral or C, contralateral phrenic burst amplitude from baseline for 60 min after axon conduction recovery in rats receiving intraspinal procaine (filled diamonds) or an equivalent duration in time controls (open triangles). No significant changes in ipsilateral or contralateral phrenic burst amplitude from baseline were detected in time controls. In rats receiving intraspinal procaine, ipsilateral phrenic amplitude was significantly increased relative to time controls at all time points following axon conduction recovery, indicating iPMF. A small, but significant increase in contralateral phrenic amplitude was observed relative to time controls at 60 min following lateralized procaine, suggesting csPMF. D, Average change in phrenic burst frequency from baseline for 60 min after axon conduction recovery in rats receiving intraspinal procaine (filled diamonds) or an equivalent duration in time controls (open triangles). Phrenic burst frequency was not significantly different than time controls at any time point post-conduction block, suggesting burst frequency facilitation was not elicited. Values presented are mean ± SEM. *Significantly different from time controls; p<0.05.