Increased thermoregulatory responsiveness in cold adapted but not in hyperthyroid hypermetabolic rats

Abstract

Cold-adapted (CA) rats, unlike non-adapted (NA) ones, give exaggerated metabolic response to acute cold exposure, with paradoxical "overshoot" core temperature (Tc) rise in the cold, and they also give enhanced hyperthermia to central injection of prostaglandin E1 (PGE1). The adaptation-dependent differences might be explained either by the high thermogenic capacity of peripheral tissues in CA rats or by differences in the central processing of regulatory signals. If high tissue metabolism sufficiently explains the extreme responses of CA animals, other hypermetabolic states (with high resting metabolic rate, RMR), e.g. hyperthyroidism, should also be accompanied by enhanced reactions. In the present study thermoregulatory responses to acute cold exposure or to PGE1 were compared in hypermetabolic CA, similarly hypermetabolic thyroxine-treated (T4) and control non-hypermetabolic NA rats (mean RMR = 8.12, 8.47 and 6.03 W kg(-1), respectively). Cold exposure was followed by paradoxical core temperature (Tc) rise of 0.5 to 0.7 degrees C only in CA rats, but by Tc fall (0.8 to 2.1 degrees C) in NA and T4 animals. Identical central stimuli (PGE1) induced larger elevations of Tc and metabolic rate in CA rats than in similarly hypermetabolic T4 or in non-hypermetabolic NA animals (mean Tc rise of 1.9 degrees C in CA vs. 0.9 degrees C in T4 and 1.0 degrees C in NA rats). Vasodilatation thresholds were also similar in NA and T4, but lowered in CA animals. A hypermetabolic status, per se, does not seem to explain the enhanced thermoregulatory responsiveness of CA animals, adaptation-induced central regulatory changes may be more important for the "overshoot" phenomenon.

The hypothermic response to bacterial lipopolysaccharide critically depends on brain CB1, but not CB2 or TRPV1, receptors

“…The experimental conditions were chosen based on the facts that the rat strain (Gordon, 1993; Ivanov et al 2003 a ) and sex (Mouihate et al 1998), as well as the ambient temperature during an experiment (Romanovsky et al 1997; Ivanov et al 2003 b ) and the prior thermal experience (e.g. the development of cold adaptation; see Petervari et al (2003), can affect the direction and magnitude of a T b response. The feeding status also influences thermoregulatory responses (Szekely, 1979; Steiner et al 2009 b ; Krall et al 2010), and at least some thermoregulatory consequences of the changes in the feeding status are TRPV1 dependent (Kanizsai et al 2009).…”