The most commonly cited descriptions of the behavioral characteristics of habituation come from two papers published almost 40 years ago (Thompson and Spencer, 1966;Groves and Thompson, 1970). In August 2007, the authors of this review, who study habituation in a wide range of species and paradigms, met to discuss their work on habituation and to revisit and refine the characteristics of habituation. This review offers a re-evaluation of the characteristics of habituation in light of these discussions. We made substantial changes to only a few of the characteristics, usually to add new information and expand upon the description rather than to substantially alter the original point.In the 20 th century, great progress was made in understanding the behavioral characteristics of habituation. A landmark paper published by Thompson and Spencer in 1966 clarified the definition of habituation, synthesized the research to date and presented a list of nine behavioral characteristics of habituation that appeared to be common in all organisms studied The history of habituation and the historical context of Thompson & Spencer's (1966) distillation are reviewed more fully in an article by Thompson (2009) that is included in this issue. This list was repeated and expanded upon by Groves and Thompson in 1970. These two papers are now citation classics and are considered to be the authorities on the characteristics of habituation. In August 2007, a group of 15 researchers (the authors of this review) who study habituation in a wide range of species and paradigms met to revisit these characteristics and refine them based on the 40 years of research since Thompson and Spencer 1966. The descriptions and characteristics from 1966 have held up remarkably well, and the revisions we have made to them were often for clarity rather than content. We made substantial changes to only a few of the characteristics, usually to add new information and expand upon the description rather than to substantially alter the original point. We restricted ourselves to an analysis of habituation; there was insufficient time for detailed discussions of the other form of non-associative learning "sensitization." Thus this review is restricted to our discussions of habituation and dishabituation (as it relates directly to habituation).Many people will be surprised to learn that, although habituation is termed "the simplest form of learning" and is well studied behaviorally, remarkably little is known about the neural mechanisms underlying habituation. Researchers who work on this form of learning believe that because habituation allows animals to filter out irrelevant stimuli and focus selectively on

Considerable evidence supports a high degree of homology between measures of PPI in rodents and humans, consistent with the use of PPI as a cross-species measure of sensorimotor gating. Multiple investigations of PPI using a variety of methods and parameters confirm that deficits in PPI are evident in schizophrenia-spectrum patients and in certain other disorders in which gating mechanisms are disturbed. In contrast to the extensive literature on clinical populations, much more work is required to clarify the degree of correspondence between pharmacological effects on PPI in healthy humans and those reported in animals.

Studies of drug effects on PPI in rats have generated four distinctive models that have utility in the identification of antipsychotic medications. Because each of these models has specific advantages and disadvantages, the choice of model to be used depends upon the question being addressed. This review should help to guide such decisions.

Studies of psychiatric disorders have traditionally focused on emotional symptoms such as depression, anxiety and hallucinations. However, poorly controlled cognitive deficits are equally prominent and severely compromise quality of life, including social and professional integration. Consequently, intensive efforts are being made to characterize the cellular and cerebral circuits underpinning cognitive function, define the nature and causes of cognitive impairment in psychiatric disorders and identify more effective treatments. Successful development will depend on rigorous validation in animal models as well as in patients, including measures of real-world cognitive functioning. This article critically discusses these issues, highlighting the challenges and opportunities for improving cognition in individuals suffering from psychiatric disorders.

Our understanding of the neural regulation of PPI has increased tremendously over the past 15 years. Progress has come in "broad strokes", and a number of important details and complex questions remain to be addressed. It is anticipated that this is a "work in progress", and that the precise models for the neural regulation of PPI will evolve substantially in the coming years.

Graham (1975) demonstrated that a weak prestimulus could effectively inhibit or facilitate the eyeblink component of the startle reflex in humans, depending on the temporal duration of the prestimulus. This study had three goals: 1) to replicate the findings of Graham, 2) to establish the reliability of this phenomenon by a test‐retest comparison, and 3) to compare the eyeblink reflex response of normal subjects with schizophrenic subjects. Seven prestimulus durations of continuous tone (from 0 to 2000 msec) were presented to 20 normal subjects and the results confirmed that maximal inhibition of eyeblink amplitude occurred in the 120 msec prestimulus condition. Increased amplitude occurred nonsignificantly when the prestimulus lasted for 2000 msec. On retest, 14 normal subjects showed a significant degree of reliability. When 20 normal subjects were compared to 12 schizophrenic subjects, significant differences in eyeblink response were found for blink amplitude and latency in the 60 msec prestimulus condition. This change is consistent with information processing “overload” theories of sensory overstimulation in schizophrenia. The blink reflex is a rather stable phenomenon and is probably altered in schizophrenia and/or by antipsychotic medication.

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Background-As a test of plausibility for the hypothesis that schizophrenia can result from abnormal brain, especially cerebral cortical, development, these studies examined whether, in the rat, disruption of brain development initiated on embryonic day (E) 17, using the methylating agent methylazoxymethanol acetate (MAM), leads to a schizophrenia-relevant pattern of neural and behavioral pathology. Specifically, we tested whether this manipulation leads to disruptions of frontal and limbic corticostriatal circuit function, while producing schizophrenia-like, regiondependent reductions in gray matter in cortex and thalamus.