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. Author manuscript; available in PMC: 2024 May 3.
Published in final edited form as: Neuron. 2023 Mar 7;111(9):1453–1467.e7. doi: 10.1016/j.neuron.2023.02.013

Figure 5. RXRα bidirectionally and cell-type-specifically regulates dose sensitivity in drug-reward associative learning.

Figure 5.

(A) HSV-mediated RXRα overexpression in NAc increased conditioned place preference (CPP) for a subthreshold (5 mg/kg) dose of cocaine (LMM-ANOVA: interaction Test:Virus: F1,44 = 10.1557, p = 0.002647, followed by Sidak’s post hoc tests).

(B) HSV-mediated RXRα overexpression in NAc increased CPP for a 7.5 mg/kg dose of morphine (LMM-ANOVA: interaction Test:Virus: F1,43 = 9.4374, p = 0.003681, followed by Sidak’s post hoc tests).

(C) AAV-mediated RXRα knockdown in NAc decreased CPP for a high (10 mg/kg) dose of cocaine (LMM-ANOVA: interaction Test:Virus: F1,41 = 5.1204, p = 0.02901, followed by Sidak’s post hoc tests).

(D) AAV-mediated NAc D1-MSN-specific RXRα overexpression increased CPP for a subthreshold (5 mg/kg) dose of cocaine (LMM-ANOVA: interaction Test:Virus: F1,44 = 28.4447, p < 0.0001, followed by Sidak’s post hoc tests).

(E) AAV-mediated NAc D2-MSN-specific RXRα overexpression did not increase CPP for a subthreshold (5 mg/kg) dose of cocaine (LMM-ANOVA: interaction Test:Virus: F1,44 = 0.0813, p = 0.7768).

(F) Chemogenetic activation of NAc MSNs using the hM3Dq DREADD rescued the effects of RXRα knockdown on cocaine CPP at a high (10 mg/kg) dose (LMM-ANOVA: interaction Test:DREADD:knockdown F1,20 = 5.4961, p = 0.0295, followed by Sidak’s post hoc tests).

Both male and female mice were used in all experiments except for chemogenetics (n = 11-12/group). Bar graphs represent mean ± SEM after combining male and female data.

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