| Popis: |
Obesity is a result of an energy imbalance based on insufficient energy expenditure relative to energy intake. Consumption of food is regulated by the central nervous system through both homeostatic and hedonic neural circuits. The present thesis examined the effect of discrete activation of agouti-related peptide (AgRP) and neuropeptide Y (NPY) neurons in the arcuate nucleus of the hypothalamus (Arc) and NPY neurons in the central nucleus of the amygdala (CeA) on various aspects of feeding behaviour. Using a chemogenetic approach - designer receptors exclusively activated by designer drugs (DREADDs) – an hM3Dq virus was injected into the Arc or CeA. As predicted, stimulation of AgRP and NPY neurons in the Arc and NPY neurons in the CeA increased food consumption. However, the results suggest that Arc and CeA regulate the consumption of food via different mechanisms. AgRP and NPY neurons in the Arc increase the consumption of food in response to homeostatic signals and leads to increased calorie-seeking behaviours, whereas NPY neurons in the CeA appear to regulate food intake hedonically. These results suggest that activation of Arc AgRP and NPY neurons produces an unpleasant feeling of hunger in the absence of food which may lead to increased calorie-seeking behaviours in animals to minimise feelings of discomfort. In contrast, activation of CeA NPY neurons in the absence of food did not induce a negative valence. Together, these findings highlight the different mechanisms regulating feeding behaviour in the Arc and CeA and may be important in understanding the underlying causes of the development of obesity. |
