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. Author manuscript; available in PMC: 2020 Jul 1.
Published in final edited form as: Mol Neurobiol. 2018 Dec 18;56(7):5241–5255. doi: 10.1007/s12035-018-1445-6

Figure 8. Linking CRMP2 phosphorylation to regulation of nociceptive ion channels in a model of neuropathic pain.

Figure 8.

Adult rats (n=6 per group) were used for these experiments 10 days after the SNI. (A) Representative immunoblots showing the presynaptic expression of CRMP2, CRMP2 pS522, CaV2.2, NaV1.7, CaV2.3 and cannabinoid receptor 1 (CB1R) in the lumbar dorsal horn of the spinal cord of SNI rats injected with (S)-Lacosamide (20μg in 5 μl, i.th.) compared to vehicle (0.1% DMSO in saline). Spinal cords (ipsilateral (i.e., injured) and contralateral (i.e., non-injured) side)) were harvested from rats 1 hour following treatment. Flotilin is used as a loading control. (B) Bar graph showing decreased CRMP2 p522 concomitant with decreased CaV2.2 and NaV1.7 levels at the presynaptic sites of lumbar dorsal horn of the spinal cord in (S)-lacosamide treated animals. Mean ± SEM, *p<0.05, Kruskal-Wallis compared to the DMSO-treated contralateral side. #p<0.05, Kruskal-Wallis compared to the DMSOtreated ipsilateral side.