The positive symptoms of acute schizophrenia and latent inhibition in humans and animals: Underpinned by the same process(es)?

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.

Keywords:

• Amphetamine
• Antipsychotic agents
• Association learning
• Haloperidol

ACKNOWLEDGEMENTS

The authors thank the Danish Agency for Science, Technology and Innovation for funding the research upon which parts of this review are based, and Rob Honey for providing valuable comments on an earlier draft of the manuscript.

Notes

¹First, the significant three-way interaction between group (healthy controls, patients), preexposure (nonpreexposed, preexposed) and set (Trials 1–5 and Trials 6–10) was not followed up by analyses contrasting control and patient groups directly. The within-group analyses presented by Gal et al. (2009) show that in Trials 1–5, control participants but not patients exhibited latent inhibition, whereas in Trials 6–10 latent inhibition was evident in patients but not controls. No analyses show that patients and controls actually differed in response times on preexposed and/or nonpreexposed trials within the two sets. Secondly, the reported analyses of the latent inhibition index (a ratio of performance in preexposed and nonpreexposed conditions) comprise t-tests contrasting the latent inhibition index between the groups within the two sets of five trials, and contrasting the latent inhibition index of patients between the two sets of trials. The authors do not report an omnibus analysis of variance showing a significant interaction between group and set, which is needed to lend credence to the claim of a latent inhibition enhancement in patients.