thermoreceptor is the part of your brain that regulates body temperature.
what part of your brain regulates body temperature?
thermoreceptor
rescuers who are trained in mountain survival techniques are taught to expect this; however, people who die from hypothermia in urban environments are sometimes incorrectly assumed to have been subjected to sexual assault.





























one explanation for the effect is a cold-induced malfunction of the hypothalamus, the part of the brain that regulates body temperature. another explanation is that the muscles contracting peripheral blood vessels become exhausted (known as a loss of vasomotor tone) and relax, leading to a sudden surge of blood (and heat) to the extremities, causing the person to feel overheated.





























section::::signs and symptoms.:terminal burrowing.
hypothermia
the role of trpv1 in the regulation of body temperature has emerged in the last few years. based on a number of trpv-selective antagonists' causing an increase in body temperature (hyperthermia), it was proposed that trpv1 is tonically active in vivo and regulates body temperature by telling the body to "cool itself down". without these signals, the body overheats. likewise, this explains the propensity of capsaicin (a trpv1 agonist) to cause sweating (i.e.: a signal to reduce body temperature). in a recent report, it was found that tonically active trpv1 channels are present in the viscera and keep an ongoing suppressive effect on body temperature. recently, it was proposed that predominant function of trpv1 is body temperature maintenance experiments have shown that trpv1 blockade increases body temperature in multiple species, including rodents and humans, suggesting that trpv1 is involved in body temperature maintenance. recently, amg 517, a highly selective trpv1 antagonist was dropped out of clinical trials due to the undesirable level of hyperthermia. a second molecule, sb-705498, was also evaluated in the clinic but its effect on body temperature was not reported. recently, it was disclosed that clinical trials of two more trpv1 antagonists, grc 6211 and ngd 8243, have been stopped. post translational modification of trpv1 protein by its phosphorylation is critical for its functionality. recent reports published from nih suggest that cdk5-mediated phosphorylation of trpv1 is required for its ligand-induced channel opening.
trpv1