The amygdaloid complex is one of the structures thought to modulate brain stimulation reward (BSR) elicited from the median forebrain bundle (MFB). Previous metabolic and behavioral data from our laboratory point to the amygdaloid cortical nuclei as key to this process. In this study, thresholds for rewarding stimulation of the MFB were determined for 42 days, 21 days following an electrolytic lesion to amygdaloid nuclei ipsilateral to the stimulation electrode, and 21 days following one applied to the contralateral amygdala. A subset of animals showed post-lesion changes in MFB frequency thresholds that were maintained if not augmented after the second lesion. These ranged from 26% to 150% compared to baseline values, among the largest ever reported to our knowledge. Interestingly, damage to anterior sites within the cortical nuclei was the most effective in producing modifications to the rewarding value of the stimulation. Equally singular was the finding that contralateral lesions tended to alter thresholds more than ipsilateral ones, confirming our earlier finding of interhemispheric connectivity in amygdaloid modulation of MFB reward signals. This interpretation was substantiated by tracking long-term metabolic activity in the amygdala using cytochrome oxidase histochemistry. The density of reaction product at damaged amygdala sites was negatively correlated (r=-0.90) with the increases in thresholds obtained at contralateral MFB loci. Together with the fact that such large lesion effects are seldom obtained, our metabolic results point to the existence of a relationship between these nuclei and reward signals generated at the MFB. Moreover, our data suggest that this communication takes place interhemispherically.
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