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Dopaminergic correlates of sensory-specific satiety in the rat : modulation by inactivation of amygdalar subregions Ahn, Soyon

Abstract

Sensory-specific satiety is a critical factor in the selection of a varied diet in humans and animals. In vivo wicrodialysis was used to investigate the modulation of dopamine (DA) efflux in the nucleus accumbens (NAc) and medial prefrontal cortex (mPFC) by the central nucleus of the amygdala (CeN) and the basolateral amygdala (BLA), and to ascertain the influence of such modulation on dopaminergic correlates of sensory-specific satiety in the rat. In each experiment, rats were given an opportunity to consume a palatable food to satiety. In a subsequent test meal, rats sampled very little of the familiar food but ingested significant amounts of a novel food. Changes in DA efflux in both the NAc and mPFC reflected this difference in food intake, indicating that DA transmission is influenced by changes in deprivation level and sensory incentive properties of food. Sensory-specific satiety was disrupted by inactivation of the CeN. Reverse-dialysis of lidocaine in the CeN resulted in ~20% decrease in basal levels of DA efflux in the NAc. Continued exposure to lidocaine during the first meal disrupted the overall expression of sensory-specific satiety and the associated changes in DA efflux in the NAc and mPFC. In contrast, inactivation of the BLA neither affected sensory-specific satiety nor its dopaminergic correlates in the NAc. Interestingly, lidocaine infusion into the BLA triggered dramatic oscillatory changes in DA efflux in the mPFC. Sensory-specific satiety was additionally assessed in rats that had been subjected to repeated cycles of food restriction and binge opportunities, a feeding regimen previously reported to lead to hyperphagia (Hagan and Moss, 1997). Cycled rats displayed normal satiety during the first meal but engaged in another vigorous bout of feeding in a second meal of the same food, which was never seen in control groups. Given that food restriction is considered to be a form of stress, which in turn is associated with sensitization of the DA system, it is conjectured that these results could be related to a similar dysfunction of the DA system, and thus, to an impairment in the control of food intake by the incentive sensory properties of food.

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