When body temperature noticeably deviates from the normal range, the functions are impaired, which could lead to heat stroke, hypothermia, and, in the worst case, death.
Scientists have identified the neurons responsible for regulating the body temperature of mammals, but what is body temperature and how is it controlled? Body temperature in humans and many other mammals is regulated at around 37 degrees Celsius, or 98.6 degrees Fahrenheit, which optimizes all regulatory functions.
When their body temperature noticeably deviates from the normal range, the functions are impaired, which could lead to heat stroke, hypothermia, and, in the worst case, death.
However, these conditions might be treated if body temperature can be artificially adjusted to the normal range.
A research group at Nagoya University in Japan has reported that a group of neurons, called EP3 neurons, in the preoptic area of the brain play a key role in regulating body temperature in mammals. The preoptic area is a part of the hypothalamus that controls the body’s vital functions.
They found that activating these neurons led to a decrease in body temperature, whereas suppressing their activity led to its increase.
The study also showed that EP3 neurons in the preoptic area play a key role in regulating body temperature by releasing GABA, or gamma-aminobutyric acid, to send inhibitory signals to dorsomedial hypothalamus (DMH) neurons to control sympathetic responses. GABA is a a major inhibitor of neuronal excitation, the study explained.
The sympathetic nervous system is constantly active at a basic level to maintain homeostasis, which is the condition of optimal functioning for the organism and includes many variables, such as body temperature and fluid balance.
The study explained that in a hot environment, signals are augmented to suppress sympathetic outputs, resulting in increased blood flows in the skin to facilitate the radiation of the body’s heat to prevent heat stroke.
However, in a cold environment, signals are reduced to activate sympathetic outputs, which promote heat production in brown adipose tissue and other organs to prevent hypothermia.
Furthermore, at the time of infection, PGE2, a mediator called prostaglandin E produced in response, acts on EP3 neurons to suppress their activity, resulting in activation of sympathetic outputs to develop fever, explained the study.
