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Feeling Nauseous? Research Suggests Your Brain Plays A Role

Date:
September 4, 2000
Source:
Ohio State University
Summary:
When it feels like you're about to lose your lunch, your brain may play as big a role as your stomach. Researchers have found that a chemical produced by the immune system directly stimulates the part of the brain that controls digestion.

COLUMBUS, Ohio - When it feels like you're about to lose your lunch, your brain may play as big a role as your stomach. Researchers have found that a chemical produced by the immune system directly stimulates the part of the brain that controls digestion.

This explains why a variety of illnesses - from cancer to the common cold - can make people feel nauseous.

"There are so many different disease states that have nothing to do with digestion, yet make a person feel lousy enough to lose his appetite," said Richard Rogers, study co-author and a professor of neuroscience at Ohio State University.

Rogers said this study may have identified the link that connects the immune, brain and digestive systems to produce the perception of illness.

The research appears in the September issue of the American Journal of Physiology: Gastrointestinal and Liver Physiology.

Rogers said that before the first hint of illness, the immune system readies itself for attack by sending out a chemical called tumor necrosis factor (TNF). Previous studies by Rogers and his colleagues found that TNF suppresses movement of food through the stomach. This study showed that TNF acts directly upon neurons in the part of the brain stem called the nucleus of the solitary tract (NST).

Cells in the NST are a critical part of the neural circuitry that regulates digestive functions, including vomiting. Rogers and his colleagues showed that when TNF acts on NST neurons, these neurons cause the stomach to stop all movement. This dramatic stomach relaxation is perceived as nausea and occurs just before a bout of vomiting.

The researchers conducted a study in rats to determine how these brainstem neurons responded to TNF. Rats were injected with levels of TNF comparable to concentrations present during a chronic infection. This TNF concentration activated NST neurons and caused digestion to stop - a condition called stasis. This leads to nausea, loss of appetite, and vomiting.

"We found that elevated levels of TNF activated the NST neurons to more readily evoke stasis," Rogers said. "And these effects lingered. Instead of eventually returning to normal, the function of NST neurons exposed to TNF was altered for quite a long time."

In this research, many NST neurons exposed to TNF did not return to a normal level of function during the course of the study. Furthermore, these neurons became overly sensitive to normal gastrointestinal events for a prolonged time.

Rogers said TNF may be released by the immune system as a response to illnesses not related to digestion, or even treatments such as radiation therapy, which also elevate TNF levels. The result could be nausea and a failure of normal digestion.

Rogers co-wrote the study with Gerlinda Hermann, a research scientist in the department of neuroscience at Ohio State, and Gregory Emch, a graduate student in the same department. This research was supported by a grant from the National Institutes of Diabetes and Digestive and Kidney Diseases.


Story Source:

The above story is based on materials provided by Ohio State University. Note: Materials may be edited for content and length.


Cite This Page:

Ohio State University. "Feeling Nauseous? Research Suggests Your Brain Plays A Role." ScienceDaily. ScienceDaily, 4 September 2000. <www.sciencedaily.com/releases/2000/09/000904092840.htm>.
Ohio State University. (2000, September 4). Feeling Nauseous? Research Suggests Your Brain Plays A Role. ScienceDaily. Retrieved October 1, 2014 from www.sciencedaily.com/releases/2000/09/000904092840.htm
Ohio State University. "Feeling Nauseous? Research Suggests Your Brain Plays A Role." ScienceDaily. www.sciencedaily.com/releases/2000/09/000904092840.htm (accessed October 1, 2014).

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