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. 2015 Feb 4;35(5):2146–2160. doi: 10.1523/JNEUROSCI.0373-14.2015

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Copyright © 2015 Frias et al.

This article is freely available online through the J Neurosci Author Open Choice option.

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Figure 8. — Photomicrographs of IC populations in the detrusor muscle. ICs were identified by anti-vimentin (green; A–C, G, H) or anti-PDGFRα (green; D–F, I, J) immunolabeling. Smooth muscle cells were labeled with phalloidin (red) and nuclei were counterstained with DAPI (blue). In the normal bladder (A, D), ICs were located within smooth muscle bundles (IC-IM) and between the bundles (IC-IB) in the normal rat bladder. One week post-SCI (B, E), there was marked upregulation of IC-IB and reduction in the IC-IM populations (*p < 0.05). Four weeks post-SCI (C, F) IC-IB presented disrupted morphology and IC-IM were apparently absent. BDNF sequestration, with intrathecal administration of TrkB-Ig2, during spinal shock (G, I) did not restore the IC populations. Prolonged administration of BDNF to SCI rats (0.7 μg/d for 4 weeks) partially restored IC-IM populations that were apparently absent in nontreated 4 week SCI rats, with little effect on IC-IB. Scale bars: 20 μm. K, Bar charts show summary quantitative analysis of detrusor IC vimentin immunolabeling after BDNF sequestration and chronic BDNF administration. Neither intervention significantly affected vimentin fluorescence (*p > 0.05).