Figure 5. LH^LEPR neurons do not regulate cocaine-context learning.

(A) Viral injection schematic.

(B) Representative images of hM3D, hM4D, and mCherry in the LH of Lepr^Cre mice. Scale bar, 500 μm.

(C) Chemogenetic LH^LEPR manipulations did not affect phase 1 sucrose CPP (post 1), but inhibition blunted the development of CPP following phase 2 training (p = 0.0136). Bonferroni post-tests for LH^LEPR:mCherry (**p = 0.0022) and LH^LEPR:hM3D mice (**p = 0.0023) in post 2 as compared to pre. Sucrose-side preference was blunted in LH^LEPR:hM4D mice as compared to LH^LEPR:mCherry (**p = 0.0049) and LH^LEPR:hM3D mice (*p = 0.0127).

(D) Chemogenetic manipulations did not affect sucrose consumption in either conditioning phase. Each group consumed more sucrose during phase 2 training (****p < 0.0001).

(E) Inhibition did not affect the induction of cocaine CPP or reinstatement following extinction. Pre, pre-test; Post, post-test; Ext, extinction test; Rnst, reinstatement test. *p < 0.05, **p < 0.01, ****p < 0.0001.

(F) No acute effects of inhibition were observed on the locomotor-stimulating effects of cocaine.

(G) LH^LEPR inhibition during daily cocaine treatment blunted increases in locomotion. *p = 0.043, **p = 0.0078.

(H and I) Prior LH^LEPR inhibition attenuated the locomotor-stimulating effects of cocaine following (H) 1 day and (I) 7 days cocaine abstinence; **p < 0.01.

Data represented as means ± SEMs; n = 5–10 mice/group.

See also Table S1 for full statistics and Figure S4.