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. Author manuscript; available in PMC: 2022 Sep 15.
Published in final edited form as: Neuropharmacology. 2021 Jul 8;196:108702. doi: 10.1016/j.neuropharm.2021.108702

Figure 2. Chemogenetic activation of the LC blunts binge-like ethanol intake in TH-ires-cre mice.

Figure 2.

I.p. CNO, but not vehicle, blunts binge-like ethanol intake in TH-ires-cre mice expressing hM3Dq DREADD (A; n=15) but not control AAV (C; n=8). I.p. CNO, but not vehicle, blunts BECs in TH-ires-cre mice expressing hM3Dq DREADD (B; n=10) but not control AAV (D; n=6). I.p. CNO, but not vehicle, blunts intake of a 3% sucrose solution in TH-ires-cre mice expressing hM3Dq DREADD (E; n=11) but not control AAV (F; n=6). Representative photomicrographs of hM3Dq DREADD virus (red, G), tyrosine hydroxylase (TH) immunohistochemistry (green, H), and hM3Dq/TH coexpression (yellow, I). For zoomed out images of DREADD expression in the LC please see Suppl. Fig. 1. Heat map of hM3Dq DREADD virus spread, with darker areas indicating similar virus expression across mice and lighter areas indicating less-common expression patterns (J). (K) Further analyses of ethanol intake data indicated that chemogenetic activation of LC TH+ neurons blunted intake in mice with High baseline ethanol intake (upper 50% of a median-split) and not in mice with Low baseline intake (lower 50% of a median-split). All values indicate mean ± SEM. Data collapsed across sexes due to absence of statistically significant sex differences. * indicates p < 0.05. Scale bar = 100 μm.