Fig. 3: Pharmacological inactivation of aPVT neurons or chemogenetic inhibition of aPVT-NAc neurons biases behavior towards food seeking.
From: A hypothalamic-thalamostriatal circuit that controls approach-avoidance conflict in rats
a (Top) Timeline of the approach-avoidance conflict test during pharmacological inactivation of aPVT neurons. (Bottom left) Representative micrograph showing the site of fluorescent muscimol microinjection into aPVT. (Bottom right) Orange areas represent the minimum (dark) and the maximum (light) spread of muscimol. b–g Muscimol inactivation of aPVT neurons (orange bars, n = 7) during the conflict test reduced the percentage of time rats spent exhibiting c avoidance (F(1, 14) = 5.59, P = 0.033) and d head-out responses (F(1, 14) = 8.58, P = 0.011), and increased e food-approach time (F(1, 14) = 3.588, P = 0.079, with a Bonferroni planned comparison P = 0.026). Animals also exhibited a trend to reduce b freezing (F(1, 14) = 2.25, P = 0.155, Bonferroni planned comparison P = 0.092). No changes were observed in f lever presses (F(1, 14) = 1.207, P = 0.29) and g latency to press (F(1, 14) = 0.28, P = 0.60), when compared to vehicle controls (gray bars, n = 9). h (Top) Timeline of the approach-avoidance conflict test during chemogenetic inhibition of aPVT-NAc neurons. (Bottom left) Representative micrograph showing the expression of hM4Di into the aPVT. Red areas represent the minimum (dark) and the maximum (light) viral expression into the aPVT. (Bottom right) Representative micrograph showing the site of microinjection of retrograde AAV-Cre-GFP into the NAc. Green areas represent the minimum (dark) and the maximum (light) viral expression into the NAc. i–n Chemogenetic inhibition of aPVT-NAc neurons (pink bars, n = 8) reduced the percentage of time rats spent exhibiting i freezing (F(1, 15) = 6.22, P = 0.024), j avoidance (F(1, 15) = 10.58, P = 0.005), and k head-out (F(1, 15) = 8.07, P = 0.012) responses, and increased l food-approach time (F(1, 15) = 7.48, P = 0.015) and m lever presses (F(1, 15) = 1.69, P = 0.21, with Bonferroni planned comparison test P = 0.040), with no changes in the n latency to press (F(1, 15) = 2.50, P = 0.13) during the conflict test, when compared to mCherry controls (gray bars, n = 9). cc corpus callosum, MD mediodorsal thalamus, 3V third ventricle, sm stria medullaris, CA3 hippocampal CA3 subregion, NAc nucleus accumbens, LV lateral ventricle, ac anterior commissure. Scale bars: 500 µm. Two-way repeated-measures ANOVA followed by Bonferroni post hoc test. Data are shown as mean ± SEM. *P < 0.05, #P between 0.05 and 0.099. See also Supplementary Figs. 6 and 7 and Supplementary Movie 3.
