Modulation by central and basolateral amygdalar nuclei of dopaminergic correlates of feeding to satiety in the rat nucleus accumbens and medial prefrontal cortex

Abstract

Current studies raise the possibility that subregions within the amygdala may interact with the mesocorticolimbic dopamine (DA) system to subserve specific psychological processes underlying food reward. The present study compared the effect of reversible inactivation of the central nucleus (CeN) versus the basolateral amygdala (BLA) on DA efflux in the nucleus accumbens (NAc) and medial prefrontal cortex (mPFC) in hungry rats that were tested in a food-devaluation procedure. During DA microdialysis experiments, lidocaine, a sodium channel blocker, was delivered via reverse dialysis into the CeN or BLA while rats were given two consecutive meals of Froot Loops. Loss of CeN function impaired the development of satiety during an initial meal and, consequently, diminished the effect of devaluation by satiety on intake of the same food during a second meal. Inactivation of the CeN was also associated with decreased basal levels of DA efflux in the NAc before food intake and attenuated increases in DA efflux related to anticipatory and consummatory aspects of feeding in both the NAc and mPFC. In contrast, inactivation of the BLA did not affect feeding behavior or DA efflux. Overall, these findings indicate that the CeN and BLA independently modulate DA transmission in both terminal regions. It is proposed that interaction between the CeN and mesocorticolimbic DA activity may be a mechanism by which hunger and satiety signals influence the value of food reward, or alternatively, a mechanism by which memory for a recently consumed food regulates food intake.

Fig. 1.

Effect of reversible inactivation of the CeN on DA efflux in the NAc associated with a food-devaluation protocol. Perfusion of the CeN with normal perfusate (A;n = 8) or perfusate containing 2% lidocaine (B; n = 8). Changes in DA efflux (line graph) and amount of food consumed (bar graph) per 10 min bins are represented as mean + SEM.Samples 4 and 13 represent periods during which a palatable food was presented behind a perforated screen, and changes in DA efflux during these periods are highlighted bydashed lines. Samples 5–8 and14–17 represent periods during which animals had access to the food. Sample 1 (white circle) represents the baseline value used as the control mean in Dunnett's tests (*p < 0.05). Comparisons between perfusate only and lidocaine conditions were conducted using Dunn's tests (†p < 0.05).

Fig. 2.

Effect of reversible inactivation of the CeN on DA efflux in the mPFC associated with a food-devaluation protocol. Perfusion of the CeN with normal perfusate (A;n = 8) or 2% lidocaine (B;n = 10). For additional explanation, see Figure 1legend. *p < 0.05; ^†p < 0.05.

Fig. 3.

Effect of reversible inactivation of the BLA on DA efflux in the NAc during a food-devaluation protocol. Perfusion of the BLA with normal perfusate (A; n = 8) or 2% lidocaine (B; n = 9). For additional explanation, see Figure 1 legend. *p < 0.05.

Fig. 4.

Location of reverse dialysis and microdialysis probes in the CeN and NAc (A), CeN and mPFC (B), and BLA and NAc (C), respectively. Vertical lines represent the dialyzing lengths of microdialysis probes (2.0 mm) in the NAc and mPFC and reverse dialysis probes in the CeN (1.2 mm) and BLA (1.8 mm). Drawings of coronal sections were adapted from Paxinos and Watson (1997). Distance from bregma is indicated.