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|Title:||The Forebrain Taste System: An Examination of the Effects of Stria Terminalis Knife-Cuts on Feeding Behaviour|
|Authors:||Black, Malcolm Thomas Richard|
|Abstract:||<p>Studies examining the etiology of obesity often focus on the relationship between taste, overeating, and the development of obesity. One animal model often used to study obesity, rats with lesions of the ventromedial hypothalamus (VMH), is popular because the degree of overeating and obesity in that animal is particularly sensitive to the taste qualities of the food the rat eats. The exaggerated sensitivity to taste in VMH rats is termed "finickiness" and is thought to contribute to the hyperphagia and obesity of this animal. The present thesis sought to identify the anatomical locus mediating finickiness. The specific hypothesis examined was that interruption of the stria terminalis (ST), a prominent component of the forebrain taste system and a fibre system destroyed in the typical VMH lesion, produces the finickiness characteristic of the VMH syndrome.</p> <p>A sham feeding paradigm was used to assess finickiness, because sham feeding allows one to measure the extent to which palatability drives feeding. I found that using sham feeding as an index, rats with ST knife-cuts were as finicky as VMH lesioned rats when consuming either sweet sucrose solutions or quinine-adulterated sucrose solutions. However, the degree of finickiness in rats with combined VMH and ST damage was equivalent to the additive effects of VMH and ST damage alone. These results lead to the conclusion that ST damage was not the locus of VMH lesion-induced finickiness.</p> <p>Nevertheless, ST knife-cuts did alter feeding; specifically ST knife-cuts produced rats which showed as much of a disturbance of sham feeding as VMH rats. Experiments 2 and 3 investigated whether the overeating of ST animals would generalize to situations when ST rats real feed. Results showed that ST rats ate normal amounts when real feeding, even though VMH rats remained hyperphagic. Thus postingestive signals from the gut, which are activated during real feeding, were sufficient to block or remove the feeding disturbance produced by interruption of the ST. However, signals from food in the gut were insufficient to block the feeding disturbance produced by VMH lesions.</p> <p>Two more experiments were conducted to determine why the hyperphagia of the ST rat during sham feeding did not generalize to real feeding. Since sham feeding may reflect motivation to eat, it was suggested that the hyperphagia of ST rats when sham feeding may reflect an increased motivation. Therefore, ST rats, VMH rats and controls were tested in a conditioned feeding procedure which provides a direct measure of food motivation. Results indicated that neither ST nor VMH rats demonstrated an increased motivation to eat.</p> <p>Experiment 5 assessed the contribution of postingestive events from the stomach to the behavioural effects noted with ST and VMH damage. Results showed that ST rats emptied a liquid meal from the stomach at the same rate as controls. However, the rate of gastric emptying was accelerated in VMH rats. It was argued that the difference in the rates at which food emptied from the stomach could account for the differences between ST and VMH rats when real feeding in spite the similarities of their behaviour during sham feeding.</p>|
|Appears in Collections:||Open Access Dissertations and Theses|
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