Abstract

Introduction. It has been suggested that the positive symptoms of acute schizophrenia are a consequence of a disruption of the process that produces latent inhibition (slower acquisition of conditioned responding after preexposure to the conditioned stimulus) and that this effect can be modelled by pro- and antipsychotic compounds in healthy participants and in nonhuman animals. This idea assumes that latent inhibition in humans and animals is underpinned by the same process(es). Method. First, we question the equivalence of human and animal latent inhibition. Second, we review the studies that have examined latent inhibition in populations with schizophrenia and in healthy populations after administration of amphetamine or haloperidol. Results. Theoretical analysis of the similarities and differences in latent inhibition effects, and the procedures used to generate them, in humans and animals renders the suggested equivalence between them unconvincing. The studies examining latent inhibition in populations with schizophrenia and in healthy populations after administration of amphetamine or haloperidol are marked by a number of methodological shortcomings and reveal discrepant results. Conclusions. The theoretical and empirical analyses provide little support for a common process underlying deficits of latent inhibition in patients exhibiting positive symptoms of acute schizophrenia, and such deficits in experimental models in healthy humans and infrahumans.

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