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. Author manuscript; available in PMC: 2015 May 1.
Published in final edited form as: Eur J Neurosci. 2014 Mar 11;39(9):1439–1454. doi: 10.1111/ejn.12516

Figure 8.

Figure 8

CCI of the sciatic nerve increased NMDA-induced NK1R internalization. Rats underwent unilateral CCI of the sciatic nerve. NK1R internalization was measured in lamina 1 neurons of segment L4. (A and B) The rats received intrathecal injections of NMDA (10 nmol) or vehicle (PBS) at the times indicated. NK1R internalization was measured in segment L4 (A) ipsilateral and (B) contralateral to CCI. (C) Comparison of the effect of intrathecal NMDA given 6 h after CCI or sham surgery. NMDA induced NK1R internalization ipsilaterally in the CCI rats but not in the sham rats. (D) CCI induced mechanical allodynia measured as responses to von Frey hairs. Data were collected from seven rats, three of which were injected with NMDA at day 7 after CCI to obtain this time point in panels A and B. (E) After CCI, rats received two intrathecal injections of vehicle (PBS), microglia inhibitors (200 nmol minocycline, 1 nmol fluorocitrate or 10 μg propentofylline), the BDNF scavenger trkB-Fc (10 μg), the trkB antagonist ANA-12 (100 nmol) or the SFK inhibitor PP2 (10 nmol). The first injection was given just after CCI and the second 3 h after CCI. All rats then received intrathecal NMDA 6 h after CCI. NMDA was always given with D-Ser (10 nmol). Numbers next to data sets indicate n. Post hoc tests (Sidak’s): *P < 0.05, **P < 0.01 ***P < 0.001 compared with vehicle (A, B and E), sham (C) or contralateral (D).