Effects of physical training on hypothalamic neuronal activation and expressions of vasopressin and oxytocin in SHR after running until fatigue.

To assess the influence of physical training on neuronal activation and hypothalamic expression of vasopressin and oxytocin in spontaneously hypertensive rats (SHR), untrained and trained normotensive rats and SHR were submitted to running until fatigue while internal body and tail temperatures were recorded. Hypothalamic c-Fos expression was evaluated in thermoregulatory centers such as the median preoptic nucleus (MnPO), medial preoptic nucleus (mPOA), paraventricular nucleus of the hypothalamus (PVN), and supraoptic nucleus (SON). The PVN and the SON were also investigated for vasopressin and oxytocin expressions. Although exercise training improved the workload performed by the animals, it was reduced in SHR and followed by increased internal body temperature due to tail vasodilation deficit. Physical training enhanced c-Fos expression in the MnPO, mPOA, and PVN of both strains, and these responses were attenuated in SHR. Vasopressin immunoreactivity in the PVN was also increased by physical training to a lesser extent in SHR. The already-reduced oxytocin expression in the PVN of SHR was increased in response to physical training. Within the SON, neuronal activation and the expressions of vasopressin and oxytocin were reduced by hypertension and unaffected by physical training. The data indicate that physical training counterbalances in part the negative effect of hypertension on hypothalamic neuronal activation elicited by exercise, as well as on the expression of vasopressin and oxytocin. These hypertension features seem to negatively influence the workload performed by SHR due to the hyperthermia derived from the inability of physical training to improve heat dissipation through skin vasodilation.

The role of peripheral transient receptor potential vanilloid 1 channels in stress-induced hyperthermia in rats subjected to an anxiogenic environment.

Anxiety resulting from psychogenic stimuli elicit stress-induced hyperthermia in rats, often called "psychogenic fever", which is part of a coordinated response to situations seen as novel or distressing. Brain transient receptor potential vanilloid 1 (TRPV1) channels modulate both thermoregulation and animal behavior; however, the role of peripheral TRPV1 channels in regulating these responses during exposure to an anxiogenic environment has not been determined. Thus, the present study aimed to investigate the involvement of abdominal TRPV1 channels in stress-induced hyperthermia and behavior in rats subjected to an unconditioned anxiety test. Desensitized rats (peripheral desensitization of TRPV1 channels with resiniferatoxin; RTX) and their respective controls were subjected to a 15-min open field (OF) test. The core body temperature (Tcore), tail skin temperature (Tskin), and rats' movements inside the arena were recorded. The OF test induced a similar increase in Tcore in both groups throughout the exposure time; however, at the recovery period, the RTX-treated rats had a slower reduction in Tcore due to lower tail skin heat loss. Tskin decreased significantly in both groups during exposure to OF but, during recovery, the RTX-treated rats showed impaired skin vasodilation. Also, RTX-treated rats entered fewer times and spent less time in the OF center square, suggesting an anxiety-related behavior. Our findings indicate that, under stressful conditions, peripheral TRPV1 channels modulate thermoregulatory and behavioral responses. The TRPV1 desensitization induces a more prolonged hyperthermic response due to lower cutaneous heat dissipation, alongside a more evident anxiety-like behavior in rats subjected to the OF apparatus.

The time-course of thermoregulatory responses during treadmill running is associated with running duration-dependent hypothalamic neuronal activation in rats.

This study evaluated the hypothalamic neuronal activation during exercise and investigated whether this activation is related to heat storage and exercise duration. Rats were subjected to a treadmill running that was interrupted at three different moments: (1) at the early phase, when minimal heat dissipation occurred due to tail vasoconstriction and the tail skin temperature (Tskin) reached its nadir; (2) at the steady-state phase, when both the Tskin and core body temperature (Tcore) plateaued at a high level (~ 20 min); and (3) at fatigue, when Tcore and Tskin were still elevated. c-Fos expression in the medial and ventromedial preoptic areas (mPOA and vmPOA), median preoptic nucleus (MnPO), paraventricular and supraoptic nucleus (PVN and SON), and septohypothalamic nucleus (SHy) was determined. Exercise increased the expression of c-Fos in all brain areas, but with different activation patterns of activation. c-Fos expression in the SHy and vmPOA was similar in all exercising groups, while in the mPOA, MnPO, and PVN, c-Fos expression gradually increased during exercise. Increased c-Fos in the SON was only evident after 20 min of exercise. Neuronal activation in the mPOA, MnPO, PVN, and SON was positively correlated with both exercise duration and heat storage. Our findings indicate that with the exception of SON, the brain areas analyzed are recruited following small changes in Tcore (~ 0.5 °C), while the SON is recruited only when Tcore reaches higher values (greater than 1.0 °C increase). c-Fos expression in the PVN, mPOA, MnPO, and SON is also influenced by exercise duration, which does not occur in the SHy and vmPOA.