Nicotine is the main addictive component of tobacco motivating continued use despite the harmful effects. World Health Organization (WHO) announced that approximately 8 million people are dead by smoking around the world. According to previous research, high intracellular calcium concentrations were important for nicotine-induced dopamine (DA) release in the brain, which normally contribute to reinforce rewarding effects. Nicotine could activate transient receptor potential ankyrin1 (TRPA1) causing calcium influx. We investigated about the link between TRPA1 and nicotine induced addictive like behaviors, using intravenous self-administration (IVSA), conditioned place preference (CPP) test, and enzyme-linked immunosorbent assay (ELISA). Pretreatment with A967079 significantly reduced nicotine self-administration and nicotine induced CPP. In reinstatement test, pretreatment with A967079 significantly reduced nicotine primed reinstatement on nicotine induced CPP. Furthermore, A967079 pretreated specifically on nucleus accumbens (NAc) attenuated nicotine induced CPP. In ELISA, the brain samples were collected from the mice injected with the drugs as with CPP schedule. Pretreatment with A967079 lessened the nicotine induced DA level increase in NAc. We identified the inhibitory effects of A967079 on nicotine induced reward and reinforcement effect, meaning that TRPA1 especially at NAc could be a therapeutic target to prevent or reduce psychological dependence for nicotine.