Skip to main content
. Author manuscript; available in PMC: 2017 Sep 1.
Published in final edited form as: Neurobiol Dis. 2016 May 1;93:226–242. doi: 10.1016/j.nbd.2016.04.010

Figure 4. PAR1 gene deletion is associated with reductions in inflammation, astrogliosis and improvements in neural preservation after experimental contusion-compression SCI.

Figure 4

Photomicrographs and associated histograms show measurements of spinal cord areas taken from H&E stained sections (A), or the percent of spinal cord area immunoreactive for GFAP (B), or Isolectin B-IR (IsoB) microglia/macrophages (C), at the 32d endpoint of each experiment. The % area at the base of the dorsal column white matter stained for PKCγ, as a measure of corticospinal axon function (D), and counts of NeuN positive neurons in the ventral horn (E), were also evaluated. In each case, measurements were made in spinal cord sections taken from the level of the injury epicenter (E), above (A), or below (B). Arrows B to E indicate an example of immunostaining in each case. In mice lacking PAR1 there was a significant increase in tissue sparring at the level of the injury epicenter (A), reductions in GFAP-IR at the injury epicenter and above (B), and reductions in IsoB-IR at the level of injury (C). In addition, PAR1−/− mice also showed significant increases in preservation of PKCγ-IR in spinal segments below the level of injury (D) and in NeuN positive ventral horn neurons above the level of injury (E) (for PAR1+/+ and PAR1−/−, n=3 uninjured and n=8 compression SCI); *P < 0.05, **P ≤ 0.01, ***P ≤ 0.001 NK). Scale Bar A = 250 µm; B to D = 100 µm and E = 20 µm.