Fig. 5.

Effects of nicotine self-administration on stress-induced neuronal activation in amygdala and hypothalamic paraventricular nucleus. Photomicrographs illustrate immunohistochemical labeling of c-Fos in coronal sections of medial amygdala (MeA; a–c) and hypothalamic paraventricular nucleus (PVN) and peri-PVN region (peri-PVN: defined as the subparaventricular zone (Spa) and the region immediately adjacent the lateral and dorsal PVN; d–f). The number of c-Fos⁺ neurons was counted in the area enclosed by dashed lines. In MeA, after sham-shock, both the saline (a) and nicotine rats (images not shown) exhibit scattered c-Fos⁺ neurons; footshock increased the expression of c-Fos in the saline group (b), and to a greater degree in the nicotine group (c). In PVN and peri-PVN, unstressed saline (a) and nicotine (images not shown) rats expressed minimal c-Fos. In the saline group (e), footshock induced c-Fos in peri-PVN, dorsal (dp) and medial parvocellular PVN (mp), but not in posterior magnocellular PVN (pm); in the nicotine group (f), foot shock induced more c-Fos in mpPVN, but less c-Fos in peri-PVN compared to the saline group. The mean ± SEM number of stress-induced c-Fos⁺ neurons is shown in panel g. *: p < 0.01, compared to the corresponding sham-shock controls. #: p < 0.01, compared to saline rats receiving footshock. Scale bar: panels a–c and d–f, 50 μm. opt: optic tract; AH: anterior hypothalamic area.