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. 2019 May 1;15:1744806919843046. doi: 10.1177/1744806919843046

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© The Author(s) 2019

Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 6. — Graphs illustrating the effect of i.t. administration of the NMDA receptor antagonists, 7-CK and MK-801 on the D-serine-induced increases in mechanical hypersensitivity, total NO production, PKC-dependent (Ser896) pGluN1 expression, and NMDA-induced spontaneous nociceptive behaviors in naïve mice. (a and b) Intrathecal administration of D-serine (500 nmol) significantly increased PWF (%) to innocuous mechanical stimuli, and this increase was significantly reduced by pretreatment with the NMDA receptor glycine antagonist, 7-chlorokynurenic acid ((a); 7-CK, 10 nmol) or the NMDA receptor channel blocker, MK-801 ((b); 10 nmol). ***P < 0.001 vs. VEH + VEH-treated group; ^##P < 0.01, ^###P < 0.001 vs. VEH + D-serine-treated group. n = 7 mice/group. (c and d) Pretreatment with 7-CK ((c); 10 nmol) or MK-801 ((d); 10 nmol) reduced the D-serine-induced increase in total NO concentration. Intrathecal administration of 7-CK and MK-801 was performed 10 min before D-ser injection and the lumbar spinal cord dorsal horn was sampled 30 min after D-serine- injection. *P < 0.05 vs. VEH + VEH-treated group; ^#P < 0.05 vs. VEH + D-ser-treated group. n = 5 mice/group. (e and f) Results of Western blot analysis showed that exogenous D-serine- increased PKC-dependent (Ser896) pGluN1 and that this increase was significantly attenuated by pretreatment with 7-CK ((e); 10 nmol) or MK-801 ((f); 10 nmol). *P < 0.05 vs. VEH + VEH-treated group; ^#P < 0.05 vs. VEH + D-ser-treated group. n = 6 mice/group. (g and h) Exogenous D-serine- significantly increased NMDA-induced spontaneous nociceptive behaviors (which included caudally directed licking, scratching, and biting). Pretreatment with 7-CK ((g); 10 nmol) or MK-801 ((h); 10 nmol) reduced the D-ser-induced increase in NMDA-induced nociceptive behaviors. **P < 0.01 vs. VEH + VEH-treated group; ^#P < 0.05, ^##P < 0.01, ^###P < 0.001 vs. VEH + NMDA-treated group; ^‡‡P < 0.01, ^‡‡‡P < 0.001 vs. D-ser + NMDA-treated group. n = 5–10 mice/group. VEH: vehicle; NMDA: N-Methyl-D-aspartate; D-ser: D-serine; n.s.: not significant; i.t.: intrathecal; PWF: paw withdrawal frequency; pGluN1, phosphorylated GluN1 subunit.