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12 - A comparison of mechanisms underlying the CS–US association and the CS–nothing association

from Current topics in latent inhibition research

Published online by Cambridge University Press:  04 August 2010

By
Thomas J. Gould
Edited by
Robert Lubow  and
Ina Weiner
Robert Lubow
Affiliation:
Tel-Aviv University
Ina Weiner
Affiliation:
Tel-Aviv University
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Summary

The ability to adapt to environmental change is essential for the survival of any organism. Adaptations to environmental change include the ability to learn associations and the ability to modify those associations. Numerous studies have demonstrated that deficits in the ability to modify or modulate learning are associated with multiple mental illnesses and disorders (Amieva, Phillips, Della, & Henry, 2004; Baron-Cohen & Belmonte, 2005; Baruch, Hemsley, & Gray, 1988; Clark & Goodwin, 2004; Kaplan et al., 2006; Lubow & Gewirtz, 1995; Lubow & Josman, 1993; Vaitl, Lipp, Bauer et al., 1999; Weiner, Schiller, & Gaisler-Salomon, 2003). Because of the strong link between mental illness and deficits in processes that modulate learning, understanding the neural substrates of these processes could facilitate development of treatments for many diseases. Latent inhibition is one process that can modulate learned associations and is also altered in patients with mental illness (see the chapters on schizophrenia in this book for an in-depth discussion).

As described in preceding chapters in this book, latent inhibition is the phenomenon in which pre-exposure to a conditioned stimulus (CS) prior to the pairing of this CS with an unconditioned stimulus (US) decreases the subsequent conditioned responses (CR). There are three phases of latent inhibition: (1) pre-exposure to the CS, (2) training (or conditioning), and (3) testing. The presence of latent inhibition is identified by comparing the degree of conditioned responding between the CS pre-exposed group and the non-pre-exposed group.

Type
Chapter
Information
Latent Inhibition
Cognition, Neuroscience and Applications to Schizophrenia
 , pp. 252 - 275
Publisher: Cambridge University Press
Print publication year: 2010

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