Fig. 6

Alcohol withdrawal anxiety accompanied by neuroinflammation further promoted binge drinking. A Experimental timeline of DID + gavage training, behavior test and measurement of alcohol drinking. B Left, schematic diagram of 2 h/4 h binge drinking after anxiety-like behavior. Right, NLRP3 KO + alcohol group mice showed a decrease in alcohol intake at 2 h and 4 h compared to the WT + alcohol group. *p < 0.05, **p < 0.01 vs WT + alcohol group, unpaired t test. n = 12 mice (WT + alcohol) and 10 mice (NLRP3 KO + alcohol). C Left, schematic diagram of two-bottle choice at 2 h, 4 h and 24 h voluntary drinking at 4 days into withdrawal. Right, voluntary alcohol intake showed no difference between WT + alcohol and NLRP3 KO + alcohol group. p > 0.05, unpaired t test. D Alcohol preference showed no difference between WT + alcohol and NLRP3 KO + alcohol group at 24 h drinking. n.s. p > 0.05, unpaired t test. E Sample images showing Nissl bodies in three groups. Scale bar = 50 μm. F The NLRP3 KO + alcohol group displayed more Nissl bodies in the mPFC and striatum compared to the WT + alcohol group. ^#p < 0.05 vs WT + alcohol group, one-way ANOVA; 3 mice per group. G The expression of IL1-β of the mPFC and striatum decreased in NLRP3 KO group compared the WT + alcohol group. *p < 0.05 vs WT group, ^#p < 0.05 vs WT + alcohol group, one-way ANOVA. H NLRP3 deficiency inhibits the expression of TNFα in the striatum. *p < 0.05 vs WT group, ^#p < 0.05 vs WT + alcohol group, one-way ANOVA. 3–6 mice per group in G and H. Data are presented as mean ± SEM