Maria C. Almeida,2 Alexandre A. Steiner,1 Luiz G S. Branco3 and Andrej A. Romanovsky1

“ A recent study of Fos protein expression in the brain [33] suggested that the DMH is also involved in the control of operant heat-avoidance behavior (moving to a reward area to trigger a breeze of cold air) . When we placed large bilateral electrolytic lesions in the DMH (Fig. 3A) , the lesions did not affect the autonomic defense of Tb against heat. However, they strongly compromised autonomic cold-defense: the same cold exposure that failed to alter Tb of the sham-lesioned rats caused marked hypothermia (P<0.001) in DMH-lesioned rats (Fig. 3B) . ”

“ In contrast, PVH-lesioned rats were allowed to select their preferred Ta and used behavioral thermoregulation (moved to a warmer environment) while responding to LPS administration in the present study. Not only does a supraneutral environment warms the body of a rat exposed to it, but it also allows the animal to mount the fever response by using skin vasoconstriction instead of the energetically expensive thermogenesis [48] , [49] . Hence, the PVH is likely involved in the circuitry of fever when the response is mounted primarily by activation of brown fat thermogenesis. ”

“ In the present study, none of the four behavioral responses studied was affected in the POA-lesioned rats (data not shown) . That the POA lacks an indispensable role in warmth- and cold-seeking behaviors induced by thermal and pharmacological stimuli is consistent with the literature. Indeed, the only mammalian thermoregulatory behavior in which involvement of the POA has been firmly established is a relaxed postural extension in response to heat exposure ”

“ In conclusion, his study identifies two neural elements essential for the cold-seeking response of rats to bacterial LPS: neuronal bodies located in the DMH and axons passing through the PVH. These are the first two landmarks on the map of the circuitry of cold-seeking behavior associated with endotoxin shock.
Methods Animals Experiments were performed in adult male Wistar rats (Harlan, Indianapolis, IN, USA) . At the time of the electrolytic or excitotoxic lesioning, the rats had a body mass of 370–400 g. ”

“ By behavioral means, humans can survive at ambient temperatures (Tas) ranging from −110°C (the surface of the moon) to 2,000°C (the air around a space shuttle as it reenters the atmosphere) while maintaining Tb within a few tenths of a degree Celsius [1] . Behavioral thermoregulatory responses vary from primitive (e.g., locomotion to a preferred Ta in a Ta gradient) to complex (e.g., maintaining Ta inside a space shuttle) . ”

“ All rats with electrolytic or excitotoxic brain lesions were examined daily for signs of dehydration and general malaise. If a rat had lost more than 15% of its body mass 24 h after lesioning or was failing to recover from its initial loss of body mass, it was injected with isotonic saline (10 ml, subcutaneously) to counteract dehydration. ”

“ Thermal stimulation was achieved by confining each rat to a short (22 cm) portion of the channel near either the warm end (Ta of ~28°C in the middle of the confinement zone) or the cold end (Ta of ~17°C in the middle of the confinement zone) of the thermogradient apparatus for 1 or 2 h. ”

“ Behavioral thermoregulation in rats with anterior hypothalamic lesions. J Comp Physiol Psychol 71: 77–82. FIND THIS ARTICLE ONLINE
Lipton J (1968) Effects of preoptic lesions on heat-escape responding and colonic temperature in the rat. Physiology & Behavior 3: 165–169. FIND THIS ARTICLE ONLINE
Romanovsky AA, Ivanov AI, Shimansky YP (2002) Selected contribution: ambient temperature for experiments in rats: a new method for determining the zone of thermal neutrality. ”

“ Excitatory amino acid receptors in the dorsomedial hypothalamus mediate prostaglandin-evoked thermogenesis in brown adipose tissue. Am J Physiol Regul Integr Comp Physiol 286: R320–R325. FIND THIS ARTICLE ONLINE
Zaretskaia MV, Zaretsky DV, DiMicco JA (2003) Role of the dorsomedial hypothalamus in thermogenesis and tachycardia caused by microinjection of prostaglandin E2 into the preoptic area in anesthetized rats. Neurosci Lett 340: 1–4. ”