Summary: Researchers have discovered a way to manage individual body temperature, mimicking the slumber method of animals like animals. By manipulating the brain’s temperature regulation system, they can induce a state of” thermoregulatory inversion” ( TI ) in rats, reducing heat production even in cold environments.
This discovery was improve the rate of survival in lethal conditions like heart attacks and strokes. The finding opens the door to medical hypothermia, which lowers metabolism and oxygen consumption and can protect cells from harm.
Important Information:
- Thermoregulatory Inversion ( TI): A novel technique that reduces heat production in response to cold.
- Brain Mechanism: The ventromedial periventricular area (VMPeA ) controls the TI state.
- People Application: TI may help regulate infarction during surgeries, metabolic problems, and brain injuries.
Origin: Oregon Health and Science University
Scientists have discovered a pioneering method to control people body temperature, potentially saving lives in emergencies in the same way a carry does it instantly lower its body temperature to endure the winter’s chill.
Researchers at Oregon Health & Science University have discovered a technique that was one day aid in the treatment of patients who are at risk for lethal events like heart attacks or strokes.
If applied in humans, who didn’t inevitably sleep, the discovery was mimic the natural capability of certain creatures to lower their body temperatures during sleep.
” The idea is to reduce the body temperature to a lower level so that organs like the head or brain don’t need as much gas, allowing them to survive the ischemia]lack of gas to tissue ] longer and improve the functional result of stroke or heart assaults”, said , Domenico Tupone, Ph. D., research associate professor of neural procedure at the OHSU School of Medicine, and mature author of the study.
When animals are cold, their body typically attempt to produce heat by shivering or burning a particular type of fat, known as colored weight. The typical thermoregulation structure of the brain, which maintains the body heat, regulates this.  ,
This method is altered in hibernating animals, such as bears and Arctic ground squirrels, during the winter so they can maintain their body temperature and avoid the harsh winters.
The body’s typical responses to warm exposure are reversed during the sleep procedure, or torpor, but that cold exposure results in a reduction in heat generation and body temperature drops.
In their research,  , published today , in the journal , Current Biology, Tupone and coworkers discovered how the mind controls this change in temperature rules. They call this approach” thermoregulatory reversal” or TI.  ,
The researchers found that by blocking a particular place in the head, called the ventromedial pericardial area, or VMPeA, they may cause this TI state in rats  , — animals that, like humans, don’t sleep normally.
During TI, exposure to cold environments stops the body from producing heat, a process known as thermogenesis, while exposure to warm increases heat production.
Their research reveals that the VMPeA acts as a” torpor switch”: When it’s active, the body reacts normally to temperature changes. However, when the activity in this part of the brain is reduced, the body shifts into TI, lowering heat production, even in the cold. This finding might cause humans to experience controlled hypothermia.
We could achieve and effectively manage therapeutic hypothermia if we had a mechanism that made us transform humans into hibernating animals, Tupone said.
These researchers demonstrated that it is possible to create a controlled hypothermia in animals that don’t hibernate by inducing the TI state in rats. This could be useful in human medicine, such as during surgeries, for treating metabolic disorders or for managing brain injuries.
In these circumstances, lowering body temperature can lessen tissue damage and speed up recovery. The goal is to induce a low temperature, low metabolism state — therapeutic hypothermia — to give patients a better chance of surviving tissue ischemia, during long surgeries, or even on long space missions.
In addition to Tupone, co-authors include:  , Shaun Morrison, Ph. D.,  , and , Pierfrancesco Chiavetta, M. D., of OHSU, and , Georgina Cano, Ph. D.,  , and , Shelby Hernan, Ph. D.,  , of the University of Pittsburgh.
Funding: This research was supported by the National Institutes of Health’s, National Institute of Neurological Disorders and Stroke under Award Numbers R01NS099234 and R01NS091066 and Office of the Director under Award Number P40OD010996.
The authors are solely responsible for the content, which does not necessarily reflect the National Institutes of Health’s official position.
The institution’s Institutional Animal Care and Use Committee ( IACUC) must review and approve any research that involves animal subjects at OHSU. The IACUC’s top priority is to safeguard the safety and health of animal research subjects.
The IACUC also reviews procedures to protect the safety of those who work with animals. The IACUC conducts a thorough review of all animal research proposals to ensure they demonstrate scientific merit and support the use of living organisms.
About this news about neuroscience and thermoregulation
Author: Angela Yeager ,
Source: Oregon Health and Science University
Contact: Angela Yeager – Oregon Health and Science University
Image: The image is credited to Neuroscience News
Original Research: Open access.
By Domenico Tupone and colleagues,” In rats, a dynorphin pathway-dependent thermoregulatory inversion is activated by the inhibition of the hypothalamic ventromedial periventricular area..” Current Biology
Abstract
In rats, a dynorphin pathway-dependent thermoregulatory inversion is activated by the inhibition of the hypothalamic ventromedial periventricular area.
CNS thermoregulatory networks increase brown adipose tissue and shivering thermogenesis to keep the body temperature at its core in mammals.
However, this canonical thermoregulatory response is replaced by a novel, emerging paradigm, thermoregulatory inversion ( TI), an alternative homeostatic state in which warm exposure stimulates thermogenesis and cold exposure inhibits thermogenesis in hibernation or torpor.
We show that the TI state is caused by either the absence of the canonical thermoregulatory integrator in the preoptic hypothalamus or the inhibition of neurons in the ventromedial periventricular area (VMPeA ) through an alternative thermoregulatory pathway in the non-torpid rat.
We have discovered a dynorphinergic input from the dorsolateral parabrachial nucleus within this pathway that is crucial for regulating the cold-evoked thermogenesis inhibition during TI.
Our findings support the possibility of pharmacologically inducing the TI state to cause therapeutic hypothermia in non-hibernating species, including humans, and reveal a novel thermosensory reflex circuit within the mammalian CNS thermoregulatory pathways.
