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The primary objective of my thesis is to explore the involvement of the amygdala, a neural structure underlying emotion, in the circuit underlying motivated behaviour as modelled by brain stimulation reward (BSR). In the first experiment, the functional links between the lateral hypothalamus (LH) and the amygdala were assessed using the metabolic marker, cytochrome oxidase. Following lesions of LH sites that supported BSR, we obtained a significant reduction of oxidative metabolism in the cortical sub-nuclei of the amygdala, suggesting their involvement in modulating the reward signals elicited from the LH. In order to test this functional relationship further, we extended our exploration of this link to another reward site, the ventral tegmental area (VTA), on both hemispheres of the brain. Following lesions to the cortical nuclei of the amygdala, some animals exhibited significant and sustained decreases in the rewarding value of LH as well as of VTA stimulation. In addition, modifications in the rewarding value of the stimulation from the MFB site contralateral to the lesion resembled ipsilateral ones, suggesting the existence of interhemispheric links in amygdaloid alteration of MFB reward signals. The nature of interhemispheric connectivity as well as a more detailed investigation of the amygdaloid sites involved in the modulation of MFB reward were explored in the final study of the thesis. Thresholds for BSR obtained from a continuum of MFB sites were tracked following serial bilateral lesions to the amygdala. One group of animals showed marked increases in thresholds that further augmented or were maintained after the second lesion. Damage to the most anterior sites encompassing cortical amygdaloid nuclei were confirmed as being more efficient than other lesions in producing substantial threshold changes. Equally exceptional was the finding that contralateral lesions were more effective than ipsilateral ones in affecting thresholds, confirming our earlier finding of interhemispheric connectivity. This interpretation was corroborated in a metabolic sub-study using cytochrome oxidase. Reaction product density within lesion sites was significantly and negatively correlated with substantial decreases in reward from the MFB electrode contralateral to them. Taken together, these data indicate that the anterior portions of the amygdaloid cortical nuclei modulate MFB reward signals. Furthermore, a significant interhemispheric communication appears to occur between these sub-nuclei in the context of reward.