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Results: 8

1.
Fig. 8.

Fig. 8. From: Deficiency of the RII? subunit of PKA affects locomotor activity and energy homeostasis in distinct neuronal populations.

Summary model. Summary of all Cre-induced RIIβ reexpression paradigms used in this study and their physiological effects. The diagram illustrates the differential regulation of locomotion and adiposity by RIIβ-PKA in striatal D2R neurons and hypothalamic GABAergic neurons. ND, not determined.

Ruimao Zheng, et al. Proc Natl Acad Sci U S A. 2013 April 23;110(17):E1631-E1640.
2.
Fig. 3.

Fig. 3. From: Deficiency of the RII? subunit of PKA affects locomotor activity and energy homeostasis in distinct neuronal populations.

Selective RIIβ expression in the striatum rescues locomotion but not adiposity. (A) Immunostaining of RIIβ in the brain of HET, RIIβlox/−, and D32-Cre/RIIβlox/− (RIIβD32) mice. (B) Immunoblots and quantification of RIIβ expression in the striatum of RIIβD32 mice compared with HET and RIIβlox/− mice. (C and D) Locomotor activity Black bar in C indicates dark cycle., (E) body weight, (F) fat mass, and (G) lean mass as determined by QMR scan, and (H) serum leptin level of HET, RIIβlox/−, and RIIβD32 mice at 20 wk of age (n = 7–16 for each group). Data are expressed as mean ± SEM. ns, not significant. *P < 0.05, **P < 0.01, ***P < 0.001, unpaired t test compared with HET control or as indicated.

Ruimao Zheng, et al. Proc Natl Acad Sci U S A. 2013 April 23;110(17):E1631-E1640.
3.
Fig. 4.

Fig. 4. From: Deficiency of the RII? subunit of PKA affects locomotor activity and energy homeostasis in distinct neuronal populations.

Effects of selective RIIβ expression in D1R or D2R neurons on locomotion and adiposity. (A) Immunostaining of RIIβ in brain sections of HET, RIIβlox/−, D1R-Cre/RIIβlox/− (RIIβD1R), and D2R-Cre/RIIβlox/− (RIIβD2R) mice. (B) Immunoblots and quantification of RIIβ level in the striatum of HET, RIIβlox/−, RIIβD1R, and RIIβD2R mice. ***P < 0.001, unpaired t test compared with HET controls (n = 3 for each genotype). (C and D) Locomotor activity (black bar in C indicates dark cycle), (E) body weight, (F) reproductive fat-pad weight, and (G) serum leptin level of HET, RIIβlox/−, RIIβD1R, and RIIβD2R mice at 16–20 wk of age (n = 8–12 for each group). Data are expressed as mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001, unpaired t test compared with HET control or as indicated.

Ruimao Zheng, et al. Proc Natl Acad Sci U S A. 2013 April 23;110(17):E1631-E1640.
4.
Fig. 5.

Fig. 5. From: Deficiency of the RII? subunit of PKA affects locomotor activity and energy homeostasis in distinct neuronal populations.

Rip2-Cre–induced RIIβ expression rescued both locomotion and adiposity. (A) Immunohistochemistry for RIIβ expression in HET, RIIβlox/−, and Rip2-Cre/RIIβlox/− (RIIβRIP2) mice. ARC, arcuate; CPu, caudate putamen; CTX, cortex; DMH, dorsomedial hypothalamus; LH, lateral hypothalamus; NAc, nucleus accumbens; Tha, thalamus; VMH, ventromedial hypothalamus. (B) Locomotor activity, (C) body weight, (D) fat mass, and (E) lean mass determined by QMR and (F) serum leptin level of HET, RIIβlox/−, and RIIβRIP2 male mice at 16 wk of age (n = 8–10 for each group). Error bars are shown as SEM. *P < 0.05, **P < 0.01, ***P < 0.001, unpaired t test compared with HET control or as indicated.

Ruimao Zheng, et al. Proc Natl Acad Sci U S A. 2013 April 23;110(17):E1631-E1640.
5.
Fig. 7.

Fig. 7. From: Deficiency of the RII? subunit of PKA affects locomotor activity and energy homeostasis in distinct neuronal populations.

AAV1-Cre–mediated RIIβ reexpression in the hypothalamus increases adiposity. (A) A representative section of the hypothalamus with AAV1-Cre-GFP injection shows GFP expression in major subregions of the hypothalamus. 3V, third ventricle; ARC, arcuate nucleus; DMH, dorsomedial hypothalamus; LH, lateral hypothalamus; VMH, ventromedial hypothalamus. (B) Immunohistochemical staining shows RIIβ expression is activated in the hypothalamus of RIIβlox/lox mice by AAV1-Cre-GFP infection but not by the control virus, AAV1-ΔCre-GFP infection. (C) Body-weight changes of male RIIβlox/lox mice with AAV1-Cre-GFP or AAV1-ΔCre-GFP injection into the hypothalamus (n = 6 for each group). AAV1-Cre was injected at 7 wk of age, and the mice were killed at 17 wk. (D) Fat mass and LBM of mice in C as determined by QMR assays at 16 wk of age. (E) Serum leptin levels of mice in C at 17 wk of age.

Ruimao Zheng, et al. Proc Natl Acad Sci U S A. 2013 April 23;110(17):E1631-E1640.
6.
Fig. 2.

Fig. 2. From: Deficiency of the RII? subunit of PKA affects locomotor activity and energy homeostasis in distinct neuronal populations.

Neuronal RIIβ expression rescues the lean and hyperlocomotor phenotypes of RIIβ KO mice. (A) Breeding strategy for generation of RIIβSyn mice with neuron-specific RIIβ reexpression. (B) Western blot analysis showed that RIIβ was expressed in brain but not in BAT or WAT of RIIβSyn mice. (C) Average locomotor activity traces of WT, RIIβlox/lox, and RIIβSyn mice. Black bars depict dark cycles. (D) Locomotor activity, (E) body weight, and (F) total fat pads of WT, RIIβlox/lox, and RIIβSyn mice (n = 5–8 for each genotype and each sex). Values represent mean ± SEM. *P < 0.05; **P < 0.01 compared with WT or as indicated. (G) Immunoblots of RIIβ in HET, RIIβlox/−, and RIIβNes mice. (H) Locomotor activity, (I) body weight, (J) reproductive fat pads, and (K) serum leptin concentrations of male HET (n = 8), RIIβlox/− (n = 6), and RIIβNes mice (n = 6) at 12 wk of age. Error bars are shown as SEM. *P < 0.05 compared with HET or as indicated.

Ruimao Zheng, et al. Proc Natl Acad Sci U S A. 2013 April 23;110(17):E1631-E1640.
7.
Fig. 6.

Fig. 6. From: Deficiency of the RII? subunit of PKA affects locomotor activity and energy homeostasis in distinct neuronal populations.

Selective RIIβ reexpression in GABAergic neurons reverses the hyperactivity and leanness of RIIβ KO mice. (A) Immunohistochemistry for RIIβ expression in the striatum and hypothalamus of Vgat-ires-Cre/RIIβlox/− (RIIβVgat) mice. 3V, third ventricle; AHA, anterior hypothalamic area; CTX, cortex; CPu, caudate putamen; DMH, dorsomedial hypothalamus; LH, lateral hypothalamus; NAc, nucleus accumbens; PVH, paraventricular hypothalamus; VMH, ventromedial hypothalamus. (B) Locomotor activity, (C) body weight, (D) fat mass, and (E) lean mass as determined by QMR and (F) serum leptin levels of HET, RIIβlox/−, and RIIβVgat male mice at 16 wk of age (n = 6–12 for each genotype). Error bars represent SEM. **P < 0.01, ***P < 0.001, unpaired t test compared with HET controls or as indicated.

Ruimao Zheng, et al. Proc Natl Acad Sci U S A. 2013 April 23;110(17):E1631-E1640.
8.
Fig. 1.

Fig. 1. From: Deficiency of the RII? subunit of PKA affects locomotor activity and energy homeostasis in distinct neuronal populations.

Generation and characterization of RIIβlox/lox mice and mice with adipocyte-specific RIIβ expression. (A) Strategy for generation of RIIβlox/lox mice. (B) Body weight and (C) QMR analysis of fat mass and (D) lean mass of RIIβlox/lox and WT control mice at 12 wk of age. (E) EE of WT and RIIβlox/lox mice was measured over 2 d and averaged and normalized to LBM. For both sexes, n = 8 for each genotype; values represent mean ± SEM. **P < 0.01. (F) Breeding strategy for generation of aP2-Cre mice with adipocyte-specific RIIβ reexpression (RIIβaP2). (G) Western blots for RIIβ in lysates from BAT, WAT, and brain of RIIβaP2 mice. β-actin was used as loading control. (H) The 72-h total locomotor activity in HET, RIIβlox/−, and RIIβaP2 mice (n = 5–8 for each group). (I–K) Body weight (I), QMR measurements of fat mass (J), and lean mass (K) of male HET (n = 16), RIIβlox/− (n = 14), and RIIβaP2 (n = 10) mice. (L) Serum leptin levels of male and female HET, RIIβlox/−, and RIIβaP2 mice at 20–22 wk of age (n = 6–14 for each group). Values represent mean ± SEM. ns, not significant. **P < 0.01; ***P < 0.001 compared with HET.

Ruimao Zheng, et al. Proc Natl Acad Sci U S A. 2013 April 23;110(17):E1631-E1640.

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