Fig. 8

NLRP3 deficiency decreases alcohol intake controlling anxiety-like behavior via modification of glutamatergic transmission in corticostriatal circuits. Top, the NLRP3 inflammasome in C57BL/6 mice is activated via binge drinking, which also increases anxiety behaviors. Optogenetic induction of LTD in corticostriatal glutamatergic transmission prevents alcohol withdrawal anxiety-like behavior. Bottom, NLRP3 deficiency decreases its downstream inflammatory factor and alcohol intake, thereby preventing anxiety-like behavior. Optogenetic induction of LTP in corticostriatal circuits reversed the NLPR3 deficiency-reduction of glutamatergic transmission and anxiety-like behavior. It highlights the role of NLRP3 in binge drinking and anxiety-like behavior