The reward-enhancement effect of nicotine in the phencyclidine model of schizophrenia: A potential factor in the comorbidity between smoking and schizophrenia

Schizophrenics smoke at a much higher rate than the general population; the reasons behind this comorbidity are currently unknown. One factor that contributes to tobacco use is the reward-enhancement effect of nicotine. Although there is a substantial amount of literature on the reward-enhancement effect of nicotine, whether or not this effect is altered in schizophrenia is unknown. This set of experiments was conducted to determine if the reward-enhancement effect of nicotine was altered in a preclinical model of schizophrenia (e.g. phencyclidine treatment). The primary reinforcing and reward-enhancement effects of nicotine were explored using three paradigms: lever-pressing for a visual stimulus, self-administration of nicotine and ultrasonic vocalizations. The paradigm used demonstrated that phencyclidine induced a deficit in the primary reinforcing and reward-enhancement effects of nicotine in the ultrasonic vocalization and self-administration. This deficit was transient in both models. Phencyclidine seemingly produced a reward-enhancement effect of its own in the lever-pressing paradigm. Withdrawal from phencyclidine led to increased reward vocalizations and increased sensitivity to stress-induced reinstatement. Together, these findings suggest that the initial reinforcing effects of nicotine are decreased by an animal model of schizophrenia but withdrawal from phencyclidine may best model differences in the reward-enhancement effect produced by an animal model of schizophrenia