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. Author manuscript; available in PMC: 2015 Aug 5.
Published in final edited form as: Cell Metab. 2014 Jun 26;20(2):333–345. doi: 10.1016/j.cmet.2014.05.021

Figure 6.

Figure 6

Role of dopamine in mediating the hypothermic response to MTII. (A) Tb, (B) nadir Tb, (C) activity, and (D) mean activity (mean of 10–60 minutes) were measured in chow-fed mice (30.0 ±0.3 g) at 22 °C pre-treated with vehicle, D1 antagonist (SCH23390, 2 mg/kg), or D2 antagonist (sulpiride, 30 mg/kg) fifteen minutes before treatment with vehicle or MTII, n=7–8/group. Activity is in arbitrary units via Mini Mitter. (E) Tb, (F) TEE, (G) RER, and (H) activity were measured at 22 °C in chow-fed mice (27.2 ±0.3 g) pre-treated with vehicle, D1and D2 antagonists (SCH23390, 2 mg/kg and sulpiride, 30 mg/kg) fifteen minutes before treatment with vehicle or MTII, n=6/group. (I) Mean arterial pressure, (J) pulse pressure, and (K) heart rate were measured in ambulating telemetered mice at 22 °C pre-treated with vehicle or D1 and D2 antagonists (SCH23390, 2 mg/kg ip and sulpiride, 30 mg/kg ip) fifteen minutes before treatment with MTII at t=0 in a crossover design, n=3–4/group. (L) chow-fed mice (29.2 ±0.3 g) at 22 °C were treated with vehicle, MTII or quinpirole at 0 h and again 2 hours later, as indicated, n=4/group. Data are mean ±SEM.