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. 2011 Dec 7;31(49):18094–18103. doi: 10.1523/JNEUROSCI.4136-11.2011

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Copyright © 2011 the authors 0270-6474/11/3118094-10$15.00/0

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Figure 7. — Morphine-induced phosphorylation of RGS9-2, formation of Gαi2/RGS9-2/14-3-3, and degradation of Gαi2 were attenuated in Nox1^−/Y. a, Morphine-induced phosphorylation of RGS9-2. The dorsal spinal cord was dissected from mice 1 h after saline or morphine administration (10 mg/kg, i.p.). Phosphorylation of RGS9-2 was detected in samples immunoprecipitated by an anti-RGS9 antibody. **p < 0.01 compared with saline-injected Nox1^+/Y; ^#p < 0.05. Values were obtained from 9 animals per group. b, Coimmunoprecipitation of RGS9-2 and Gαi2 with 14-3-3 proteins. The dorsal spinal cord was dissected from mice 2 h after saline or morphine injection. RGS9-2 and Gαi2 were detected in samples immunoprecipitated by an anti-14-3-3 antibody. **p < 0.01 compared with saline-injected Nox1^+/Y; ^##p < 0.01. Values were obtained from 7 to 8 animals per group. c, Levels of Gαi2 protein. The dorsal spinal cord was dissected from mice at 24 h after saline or morphine injection, and the synaptosomal fraction was subjected to immunoblotting. **p < 0.01 compared with saline-injected Nox1^+/Y. Values were obtained from 8 animals per group.