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Cocaine addiction causes serious health problems, and no effective treatment is available yet. We previously identified a genetic risk variant for cocaine addiction in the  PLCB1  gene and found this gene upregulated in postmortem brains of cocaine abusers and in human dopaminergic neuron-like cells after an acute cocaine exposure. Here, we functionally tested the contribution of the  PLCB1  gene to cocaine addictive properties using  Plcb1 +/− mice. First, we performed a general phenotypic characterization and found that  Plcb1 +/− mice showed normal behavior, although they had increased anxiety and impaired short-term memory. Subsequently, mice were trained for operant conditioning, self-administered cocaine for 10 days, and were tested for cocaine motivation. After extinction, we found a reduction in the cue-induced reinstatement of cocaine-seeking behavior in  Plcb1 +/− mice. After reinstatement, we identified transcriptomic alterations in the medial prefrontal cortex of  Plcb1 +/− mice, mostly related to pathways relevant to addiction like the dopaminergic synapse and long-term potentiation. To conclude, we found that heterozygous deletion of the  Plcb1  gene decreases cue-induced reinstatement of cocaine-seeking, pointing at PLCB1 as a possible therapeutic target for preventing relapse and treating cocaine addiction.

Reduced cue-induced reinstatement of cocaine-seeking behavior in Plcb1 +/− mice