Fig. 4.

Inactivation of the vHipp-NAc normalizes dopamine population activity in MAM-treated rats. The schematic depicting the strategy used for pathway inhibition is shown in a, b. An adeno-associated virus that expressed the Gi DREADD was injected into the vHipp. At the time of testing, CNO was injected directly into the NAc (a) or mPFC (b). Cartoon showing the location of the CNO injection and micrograph of representative section are shown in c, d. DREADD expression in pyramidal cells of the vHipp was confirmed using immunohistochemistry and a representative image is shown in e⁷⁰. n = 3 rats per group. Scale bar is 50 microns. MAM-treated animals show an increase in the number of spontaneously active dopamine cells per track in the VTA compared to saline controls. Chemogenetic inactivation of vHipp afferents to the NAc completely abolishes the MAM-induced increase in dopamine population activity (f). Neither firing rate (g) nor the percentage of action potentials fired in bursts (h) were affected by MAM treatment or pathway inhibition. n = 5 rats per group. Asterisk is significantly different from saline/GFP; +plus is significantly different than MAM/GFP. The MAM-induced increase in dopamine cell population activity is not affected by inhibition of the vHipp to mPFC pathway (i). Neither MAM treatment nor pathway inhibition affect firing rate (j). The percentage of action potentials fired in a burst pattern was decreased by vHipp-mPFC pathway inhibition in both the saline- and MAM-treated animals (k). n = 4–5 rats per group. Asterisk is significantly different from saline; +plus is significantly different than GFP. All data were analyzed using Two-Way ANOVA and Holm–Sidak tests. Data are shown as mean ± SEM