Latent inhibition refers to the observation that under specific conditions, nonreinforced preexposure (PE) to a stimulus retards the efficacy with which this stimulus is conditioned when paired with reinforcement, compared to a nonpreexposed (NPE) stimulus. The pharmacology of LI has been almost exclusively associated with the use of LI as an animal model of schizophrenia, and therefore largely overlaps the pharmacology of schizophrenia.
As detailed in our chapter on neural substrates of LI, the widely held notion that nonreinforced stimulus preexposure reduces attention to or salience of stimuli has served to link LI to attentional processing in schizophrenia. Specifically, because schizophrenia is characterized by an inability to filter out, or ignore, irrelevant or unimportant stimuli, abnormal LI was proposed as a tool for modeling deficient attention in schizophrenia (Solomon, Crider, Winkelman et al.,1981; Weiner, Lubow, & Feldon, 1981, 1984, 1988). Here we will focus on our use of LI for the development of pharmacological animal models related to schizophrenia and the identification of viable antipsychotic/anti-schizophrenia medications. Based on our initial pharmacological data, we adopted in our pharmacological investigations a view of LI that distinguished between the acquisition of LI (learning to ignore the nonreinforced stimulus in preexposure) and the expression of LI (subsequent expression of this learning in conditioning) (Weiner, Feldon, & Katz, 1987; Weiner et al., 1984, 1988). This view of LI has been elaborated in the switching model of LI (Weiner, 1990, 2003; Weiner & Feldon, 1997), and has guided our use of LI for modeling schizophrenia.