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Similarly, for the CCI model, Δ p ^ was 2.6%, 4.7%, and 0.7% when the CCI, age, and sex were removed, respectively.
HBO increased the expression of PKG1 in the dorsal horn of the CCI model.
We established CCI model by ligating sciatic nerve as described by Ding Y [32] for mirroring features of clinical neuropathic pain.
The CCI model possesses characteristics of peripheral and central sensitization, similar to clinical features of NP, and has been widely used in studies on pain [20].
Similarly, in the CCI model a small population of capsaicin-sensitive neurons developed cold sensitivity after injury.
Our data indicate that an alteration in the number of cold sensitive DRG neurons is not a mechanism for cold allodynia in the CCI model of neuropathic pain.
This reduction was greater than the reduction observed for the CCI model.
Therefore, the PRI model has a better ability to reclassify patients than the CCI model.
The CCI analysis was compared with sham surgery for the important consideration of a craniotomy effect in the CCI model.
The C-statistic was marginally better for the PRI model than for the CCI model (91.5 versus 91.3).
Studies with various severities of the CCI model have shown increased BrdU incorporation during the first few days postinjury (Ramaswamy et al., 2005; Radomski et al., 2013).
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