Fig. 4.

Evaluation of role of medial shell D1R signaling in reward–related food intake. a Sweet milk intake elicited neuronal activation mostly in D1R+ and less in D1R− cells in the medial shell. The representative pictures show Fos-immunoreactive cells (brown nuclei) with positive (left, dense silver grain accumulation) and negative (right, few scattered grains at background level) D1R mRNA labeling. b Fos activation in the accumbens nucleus in relation to the amount of consumed sweet milk. As before (Fig. 2b), a strong correlation was established between the consumed quantity and the number of Fos+ neurons. Separate analysis of D1R-positive and D1R-negative Fos cells verified that only D1R-bearing neurons code reward-related information. Solid and dashed lines show linear regressions and 95% confidence intervals, respectively, see correlation coefficients on the graphs, *p < 0.05, n = 6. c Influence of local stimulation of medial shell neurons with D1 agonist SKF-82958 on SCM intake and neuronal activation in the LHA. Top: Illustration of microinjection sites for different doses of SKF-82958. The diagrams were adopted from the Atlas of Paxinos and Watson [24] and illustrate frontal section levels rostral to Bregma in mm as indicated. Bottom: SCM consumption was attenuated markedly by the treatment independently from doses applied. d The number of Fos+ cells in the lateral hypothalamic area after SCM intake. The different doses reduced cell activation in a similar manner in both investigated areas. Top: Fos+ cell nuclei appear as black dots on the representative pictures. Bottom: Results of the quantitative analyses, n = 6,*p < 0.05 vs. saline. Data are presented as means ± SEM. c core, sh shell, LH lateral hypothalamic, PF perifornical regions of the lateral hypothalamic area