Extended Data Fig. 1: Endogenous MOPR activation in mNAcSh is necessary for potentiating state-dependent consummatory behavior.
From: An endogenous opioid circuit determines state-dependent reward consumption
a. Placement map of each microinjector tip (blue = intake suppression compared to vehicle-deprived, green = intake enhancement compared to vehicle-deprived). b. Schematic of vehicle (ACSF, gray, top) or drug (CTAP, blue, bottom) microinjections into areas surrounding nucleus accumbens (NAc) medial shell. c. CTAP (blue) had no effect on ad libitum or hunger enhanced intake compared to vehicle (gray) control days when injections were outside NAc medial shell (n = 8). d. In situ hybridization of Pdyn, Penk and Oprm1 in NAc medial shell (scale bar = 200µm). e, f. Quantification of MOPR expression in mNAcSh. g. Schematic of Oprm1fl/fl x Pdyn-Cre mouse line cross. h, i. In situ hybridization (h) and quantification (i) of Pdyn, Penk and Oprm1 in NAc medial shell (scale bar = 200 µm) in Oprm1fl/fl x Pdyn-Cre mouse line. j. Loss of MOPRs on Pdyn-Cre+ neurons did not disrupt normal ad libitum or food deprived enhanced intake compared to Pdyn-Cre- littermate control mice (n = 9 Cre-, 10 Cre+). k and l. In situ hybridization (k) and quantification (l) of Pdyn, Penk and Oprm1 in NAc medial shell (scale bar = 200 µm) in Oprm1fl/fl x Penk-Cre mouse line. m. Schematic and image of rAAV5-CMV-Cre-GFP injections into NAc medial shell of Oprm1fl/fl mice. n. Schematic of combined viral spread map of local MOPR deletion. o. Schematic (top) and image (bottom) of AAV2retro-CMV-myc-NLS-Cre or AAV2retro-GFP-Cre injections into NAc (left); retrogradely labeled cells in dorsal raphe nucleus (right). All error bars represent ± SEM and n = biologically independent mice or cells (f, i, l). Medians marked with orange bar. Post hoc p-values are derived from Two-way ANOVA with Sidak multiple comparisons (c, j).
