Abstract: P. F. Lovibond and D. R. Shanks (2002) suggested that all forms of classical conditioning depend on awareness of the stimulus contingencies. This article considers the available data for eyeblink classical conditioning, including data from 2 studies (R. E. Clark, J. R. Manns, & L. R. Squire, 2001; J. R. Manns, R. E. Clark, & L. R. Squire, 2001) that were completed too recently to have been considered in their review. In addition, in response to questions raised by P. F. Lovibond and D. R. Shanks, 2 new analyses of data are presented from studies published previously. The available data from humans and experimental animals provide strong evidence that delay eyeblink classical conditioning (but not trace eyeblink classical conditioning) can be acquired and retained independently of the forebrain and independently of awareness. This conclusion applies to standard conditioning paradigms; for example, to single-cue delay conditioning when a tone is used as the conditioned stimulus (CS) and to differential delay conditioning when the positive and negative conditioned stimuli (CS+ and CS-) are a tone and white noise.

Abstract: The field of animal cognition is strongly rooted in the philosophy of mind and in the theory of evolution. Despite these strong roots, work during the most famous and active period in the history of our science-the 1930s, 1940s, and 1950s-may have diverted us from the very questions that were of greatest initial interest to the comparative analysis of learning and behavior. Subsequently, the field has been in steady decline despite its increasing breadth and sophistication. Renewal of the field of animal cognition may require a return to the original questions of animal communication and intelligence using the most advanced tools of modern psychological science. Reclaiming center stage in contemporary psychology will be difficult; planning that effort with a host of strategies should enhance the chances of success.

Abstract: About 2-3% of all children are affected by mental retardation, and genetic conditions rank among the leading causes of mental retardation. Alterations in the information encoded by genes that regulate critical steps of brain development can disrupt the normal course of development, and have profound consequences on mental processes. Genetically modified mouse models have helped to elucidate the contribution of specific gene alterations and gene-environment interactions to the phenotype of several forms of mental retardation. Mouse models of several neurodevelopmental pathologies, such as Down and Rett syndromes and X-linked forms of mental retardation, have been developed. Because behavior is the ultimate output of brain, behavioral phenotyping of these models provides functional information that may not be detectable using molecular, cellular or histological evaluations. In particular, the study of ontogeny of behavior is recommended in mouse models of disorders having a developmental onset. Identifying the role of specific genes in neuropathologies provides a framework in which to understand key stages of human brain development, and provides a target for potential therapeutic intervention.

Abstract: The distinction between psychology and praxics provides a clear answer to the question of animal cognition. As Griffin and others have noted, the kinds of behavioral phenomena that lead psychologists to speak of cognition in humans are also observed in nonhuman animals, and therefore those who are convinced of the legitimacy of psychology should not hesitate to speak of and to attempt to study animal cognition. The behavior of organisms is also a legitimate subject matter, and praxics, the study of behavior, has led to significant advances in our understanding of the kinds of behaviors that lead psychologists to speak of cognition. Praxics is a biological science; the attempt by students of behavior to appropriate psychology has been misguided. Generativity theory is an example of a formal theory of behavior that has proved useful both in the engineering of intelligent performances in nonhuman animals and in the prediction of intelligent performances in humans.

Abstract: Anomalies in the laterality of numerous neurocognitive dimensions associated with schizophrenia have been documented, but their role in the etiology and early development of the disorder remain unclear. In the study of normative neurobehavioral organization, animal models have shed much light on the mechanisms underlying and the factors affecting adult patterns of both functional and structural asymmetry. Nonhuman species have more recently been used to investigate the environmental, genetic, and neuroendocrine factors associated with developmental language disorders in humans. We propose that the animal models used to study the basis of lateralization in normative development and language disorders such as dyslexia could be modified to investigate lateralized phenomena in schizophrenia.