Rats give clue to nausea linked to cancer treatmentsPublished On: Sun, Oct 7th, 2012 | Cancer Research | By BioNews
Many drugs that target cancers cause nausea, a common and distressing side-effect with a sensation of unease and discomfort in the upper stomach, say researchers.
Now researchers with the help of some “disgusted” rats have identified the mechanism that causes this, possibly opening the way to more effective management of nausea and vomiting linked with cancer treatment.
Linda Parker, professor of behavioural neuroscience, University of Guelph, who conducted the research with doctoral student Katharine Tuerke and Cheryl Limebeer, said: “Although everyone has experienced nausea at some point, its neurobiology is poorly understood due to a lack of animal models,” the Journal of Neuroscience reported.
“We know about vomiting. The vomiting reflex is very well characterized, but the experience of nausea is something that little is known about. How is it generated? Where is it generated?” Parker added, according to a Guelph statement.
Although rats can’t vomit, they do display a disgust reaction called gaping when re-exposed to a taste that made them feel nauseous in the past. Therefore, these gaping reactions in rats provide a model to understand brain mechanisms that produce nausea in humans.
Using this gaping model, Guelph researchers, along with University of Toronto professor Paul Fletcher, discovered that serotonin release in the visceral insular cortex may be responsible for the sensation of nausea.
The insular cortex is a site of taste and illness input in the brain.
Researchers first demonstrated that depletion of serotonin in the entire insular cortex prevented the nausea-induced gaping reactions in rats, suggesting that serotonin activation in this region is necessary for the production of nausea.
Double Dissociation between Regulation of Conditioned Disgust and Taste Avoidance by Serotonin Availability at the 5-HT3 Receptor in the Posterior and Anterior Insular Cortex, Katharine J. Tuerke,Cheryl L. Limebeer,Paul J. Fletcher, and Linda A. Parker, The Journal of Neuroscience, 3 October 2012, 32(40): 13709-13717; doi: 10.1523/JNEUROSCI.2042-12.2012