The contribution of the mouse tail to thermoregulation is modest

Abstract

Understanding mouse thermal physiology informs the usefulness of mice as models of human disease. It is widely assumed that the mouse tail contributes greatly to heat loss (as it does in rat), but this has not been quantitated. We studied C57BL/6J mice after tail amputation. Tailless mice housed at 22°C did not differ from littermate controls in body weight, lean or fat content, or energy expenditure. With acute changes in ambient temperature from 19 to 39°C, tailless and control mice demonstrated similar body temperatures (Tb), metabolic rates, and heat conductances and no difference in thermoneutral point. Treatment with prazosin, an α1-adrenergic antagonist and vasodilator, increased tail temperature in control mice by up to 4.8 ± 0.8°C. Comparing prazosin treatment in tailless and control mice suggested that the tail's contribution to total heat loss was a nonsignificant 3.4%. Major heat stress produced by treatment at 30°C with CL316243, a β3-adrenergic agonist, increased metabolic rate and Tb and, at a matched increase in metabolic rate, the tailless mice showed a 0.72 ± 0.14°C greater Tb increase and 7.6% lower whole body heat conductance. Thus, the mouse tail is a useful biomarker of vasodilation and thermoregulation, but in our experiments contributes only 5-8% of whole body heat dissipation, less than the 17% reported for rat. Heat dissipation through the tail is important under extreme scenarios such as pharmacological activation of brown adipose tissue; however, non-tail contributions to heat loss may have been underestimated in the mouse.

Keywords: ambient temperature; body temperature; energy expenditure; heat conductance; tail.

Fig. 1.

No effect of tail loss on growth. Body weight (A; BW), lean mass (B), fat mass (C), food intake (D), and total energy expenditure (E; TEE) by mass balance were measured in C57BL/6J mice. Littermate control and tailless male and female mice were singly housed and fed a chow diet. Data are means ± SE, n = 7–9 mice/group.

Fig. 2.

Effect of ambient temperature (Ta) on tailless mice. Light and dark phase core body temperature (Tb) and physical activity (A and B), difference between dark and light Tb (C), and Tb span (the 95th minus the 5th percentile) (D) in male control and tailless mice. Tb and activity were monitored continuously by telemetry for 72 h in singly housed mice at Ta of 22, 31, or 34.4°C, as indicated. Data are means ± SE, n = 6–26 mice/group (male). E and F: control and tailless mice previously housed at 22°C or 30°C for 10 days were acclimated to indirect calorimetry chambers for 2 days and then exposed to a range of Ta. Total energy expenditure (TEE), Tb, and heat conductance were analyzed by mixed model segmented regression (see materials and methods and Ref. 44). For visual clarity, only Ta plateau mean ± SE data points are depicted; however, all data were included in the regression models. Complete regression results are in Table 3.

Fig. 3.

Prazosin-induced vasodilation increases heat loss. A: infrared thermography (IR) of a mouse pretreatment (top) or 70 min after prazosin (bottom). Skin surface temperature measurements are on the tail (1 cm from base, T_Tail), shaved lumbar (T_Lumbar), and interscapular (T_BAT) areas and unshaved fur (T_Fur) between the T_Lumbar and T_BAT areas. B: IR images 70 min after treatment with prazosin or vehicle (water). Prazosin increased temperature of the feet (arrows) but not the ears (asterisks). C: correlation between T_Lumbar and intraperitoneal temperature (Tb) measured concurrently. Solid line is regression T_Lumbar = (0.88 ± 0.02)Tb + (3.31 ± 0.65), R² = 0.80, df = 608, n = 14 mice (mixed sex). Dotted reference line is T_Lumbar = Tb. D: T_Tail after treatment with the indicated doses of prazosin, n = 5 mice (mixed sex). E: prazosin dose response. ΔT_Tail is the change from baseline, calculated as T_Tail mean of 10 to 170 min minus T_Tail mean of −40 to −10 min, (treatment_10to170 – baseline_−40to−10). F and G: effect of prazosin on T_Tail, T_Lumbar, T_BAT, T_Fur, and Tb in control mice. The 22°C ambient temperature (Ta) is indicated, n = 9 or 10 mice/group (mixed sex). H–L: drug effect was calculated as the change from baseline (treatment_5to110 – baseline_−65to−10). Prazosin and vehicle effect were compared by unpaired t test. M–T: effect of prazosin on total energy expenditure (TEE), Tb, heat loss, and heat conductance of control and tailless mice. Drug effect was calculated as the vehicle-corrected change from baseline [(prazosin_60to180 – prazosin_{−150to−30}) – (vehicle_60to180 – vehicle_{−150to−30})]. n = 10–13 mice/group (male). Data are means ± SE, compared by unpaired t test. Prazosin dose was 2.5 mg/kg, ip, except in dose response.

Fig. 4.

Effect of a β3-adrenergic agonist, CL316243, on skin and body temperatures. A and B: effect of CL316243 (0.1 mg/kg, ip) or vehicle (saline) on interscapular (T_BAT), lumbar (T_Lumbar), tail (T_Tail), and unshaved fur (T_Fur) surface temperatures and intraperitoneal temperature by telemetry (Tb) in control mice. The 22.5°C ambient temperature (Ta) is indicated. C–G: drug effect was calculated as the change from baseline (treatment_5to115 – baseline_−45to−5). Data are means ± SE, n = 7 mice/group (mixed sex), compared by unpaired t test.

Fig. 5.

Effect of CL316243 on the thermal metabolism. Mice were treated with CL316243 (0.1 mg/kg, ip) or vehicle (saline) at 22°C (A–D) or 30°C (E–H) and the effect on total energy expenditure (TEE), body temperature (Tb), heat loss, and heat conductance were measured. I–L: drug effect was calculated as the vehicle-corrected change from baseline [(CL316243_60to180 – CL316243_{−150to−30}) – (vehicle_60to180 – vehicle_{−150to−30})]. Data are means ± SE, n = 5 or 6 mice/group (22°C) or n = 10 or 11 mice/group (30°C) (male); control and tailless were compared by unpaired t test.