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. Author manuscript; available in PMC: 2022 Oct 1.

Published in final edited form as: Pain. 2021 Oct 1;162(10):2499–2511. doi: 10.1097/j.pain.0000000000002353

Figure 5. — Activation of PKCδ in the trigeminal ganglion (TG) neurons in chronic NTG-treated mice. Immunohistochemistry analysis showed plasma membrane translocation of PKCδ (A), but not PKCε (B), on Day 7 in TG of chronic NTG-treated mice. The fluorescent intensity of PKC isoform across representative cells (indicated by dashed arrows) is shown. Green, PKCδ; Cyan, PKCε; Red, NeuN; Blue, DAPI. Scale bars: 50 μm. n = 15 slices from 3 mice.

Figure 5. — Activation of PKCδ in the trigeminal ganglion (TG) neurons in chronic NTG-treated mice. Immunohistochemistry analysis showed plasma membrane translocation of PKCδ (A), but not PKCε (B), on Day 7 in TG of chronic NTG-treated mice. The fluorescent intensity of PKC isoform across representative cells (indicated by dashed arrows) is shown. Green, PKCδ; Cyan, PKCε; Red, NeuN; Blue, DAPI. Scale bars: 50 μm. n = 15 slices from 3 mice.