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Am J Physiol Regul Integr Comp Physiol 251: R575-R581, 1986;
0363-6119/86 $5.00
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AJP - Regulatory, Integrative and Comparative Physiology, Vol 251, Issue 3 575-R581, Copyright © 1986 by American Physiological Society

ARTICLES

Area postrema lesions: cause of overingestion is not altered visceral nerve function

G. L. Edwards and R. C. Ritter

Rats with lesions of the area postrema and the immediately subjacent nucleus of the solitary tract (AP lesions) ingest greater quantities of palatable foods than intact rats. Because AP lesions destroy some abdominal vagal sensory terminals and may damage vagal motor neurons as well, it is possible that lesion-induced alteration of vagal function causes overingestion of palatable foods. To test this hypothesis, we have examined ingestion of a highly palatable solid food by AP- and sham-lesioned rats with total subdiaphragmatic vagotomies and examined ingestion of a highly palatable sucrose solution by AP- and sham-lesioned rats with open gastric fistulas (sham feeding). Vagotomy in sham-lesioned rats failed to cause overingestion of palatable food. Furthermore, vagotomy in AP-lesioned rats did not abolish their overingestion of palatable food, although AP lesion-induced overingestion was attenuated by vagotomy. Finally, sham-feeding AP-lesioned rats consumed significantly more sucrose solution than sham-lesioned rats. These results indicate that overingestion of palatable foods and solutions by AP-lesioned rats is not due to impaired abdominal visceral afferent function and probably is not due to altered vagal efferent function. The data are consistent with our previous suggestion that overingestion by AP-lesioned rats results from a primary change in responsiveness to orosensory cues.


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