While we agree that the cultural imbalance in the recruitment of participants in psychology experiments is highly detrimental, we emphasize the need to complement this criticism with a warning about the “weirdness” of some cross-cultural studies showing seemingly deep cultural differences. We take the example of economic games and suggest that the variety of results observed in these games may not be due to deep psychological differences per se, but rather due to different interpretations of the situation.

The peripheral nervous system (PNS) has classically been separated into a somatic division composed of both afferent and efferent pathways and an autonomic division containing only efferents. J. N. Langley, who codified this asymmetrical plan at the beginning of the twentieth century, considered different afferents, including visceral ones, as candidates for inclusion in his concept of the “autonomic nervous system” (ANS), but he finally excluded all candidates for lack of any distinguishing histological markers. Langley's classification has been enormously influential in shaping modern ideas about both the structure and the function of the PNS. We survey recent information about the PNS and argue that many of the sensory neurons designated as “visceral” and “somatic” are in fact part of a histologically distinct group of afferents concerned primarily autonomic function. These afferents have traditionally been known as “small dark” neurons or B-neurons. In this target article we outline an association between autonomic and B-neurons based on ontogeny, cell phenotype, and functional relations, grouping them together as part of a common reflex system involved in homeostasis. This more parsimonious classification of the PNS, made possible by the identification of a group of afferents associated primarily with the ANS, avoids a number of confusions produced by the classical orientation. It may also have practical implications for an understanding of nociception, homeostatic reflexes, and the evolution of the nervous system.

Giulio Tononi's integrated information theory (IIT) proposes explaining consciousness by directly identifying it with integrated information. We examine the construct validity of IIT's measure of consciousness, phi (Φ), by analyzing its formal properties, its relation to key aspects of consciousness, and its co-variation with relevant empirical circumstances. Our analysis shows that IIT's identification of consciousness with the causal efficacy with which differentiated networks accomplish global information transfer (which is what Φ in fact measures) is mistaken. This misidentification has the consequence of requiring the attribution of consciousness to a range of natural systems and artifacts that include, but are not limited to, large-scale electrical power grids, gene-regulation networks, some electronic circuit boards, and social networks. Instead of treating this consequence of the theory as a disconfirmation, IIT embraces it. By regarding these systems as bearers of consciousness ex hypothesi, IIT is led toward the orbit of panpsychist ideation. This departure from science as we know it can be avoided by recognizing the functional misattribution at the heart of IIT's identity claim. We show, for example, what function is actually performed, at least in the human case, by the cortical combination of differentiation with integration that IIT identifies with consciousness. Finally, we examine what lessons may be drawn from IIT's failure to provide a credible account of consciousness for progress in the very active field of research concerned with exploring the phenomenon from formal and neural points of view.

Although cognitive scientists have learned a lot about concepts, their findings have yet to be organized in a coherent theoretical framework. In addition, after twenty years of controversy, there is little sign that philosophers and psychologists are converging toward an agreement about the very nature of concepts. Doing without Concepts (Machery 2009) attempts to remedy this state of affairs. In this article, I review the main points and arguments developed at greater length in Doing without Concepts.

In addition to the infant cry being a signal for attention, it may also be a critical component of the early formation of attachments with caregivers. We consider the complex development of that attachment, which involves reciprocal interactive signaling and a host of evolutionarily conserved caregiver factors.

Lucid dreaming provides a test case for theories of dreaming. For example, whether or not “loss of self-reflective awareness” is characteristic of dreaming, it is not necessary to dreaming. The fact that lucid dreamers can remember to perform predetermined actions and signal to the laboratory allows them to mark the exact time of particular dream events, allowing experiments to establish precise correlations between physiology and subjective reports, and enabling the methodical testing of hypotheses.

[Hobson et al.; Solms]

Why did Homo erectus begin to craft symmetric tools? A parsimonious account assumes that preference for symmetry is inherent in all visual systems. This preference can be explained by a broader preference for perceptual fluency. The perceptual fluency account does not assume that selection for mate health or the production of symbolic art is a prerequisite for symmetry preference.

Cognitive deficits were produced in rats by different methods of damaging the brain: chronic ingestion of alcohol, causing widespread damage to diffuse cholinergic and aminergic projection systems; lesions (by local injection of the excitotoxins, ibotenate, quisqualate, and AMPA) of the nuclei of origin of the forebrain cholinergic projection system (FCPS), which innervates the neocortex and hippocampal formation; transient cerebral ischaemia, producing focal damage especially in the CA1 pyramidal cells of the dorsal hippocampus; and lesions (by local injection of the neurotoxin, colchicine) of the granule cells of the dentate gyrus. Following chronic alcohol or lesions of the FCPS, transplants of cholinergically rich fetal brain tissue into the terminal areas (neocortex and/or hippocampus) restored performance almost to control levels, with a time course consistent with growth of the transplants and integration with host tissue; transplants of cholinergically poor fetal tissue (hippocampus) were without effect, as were transplants of cholinergically rich tissue into the region containing the nuclei of origin of the FCPS. Grafts of primary cells enriched in glia and cultured neuroblastoma cells into the terminal areas of the FCPS were equally effective, suggesting that there are multiple mechanisms by which neural transplants can restore cognitive function following diffuse cholinergic damage. In contrast, after ischaemia- or neurotoxin-induced damage to CA1 or dentate granule cells respectively, cholinergically rich fetal transplants into the damaged hippocampal formation were ineffective in restoring performance. After ischaemic damage, however, performance was restored by suspension grafts of CA1 cells but not by transplants containing CA3 pyramidal cells or granule cells; and after colchicine damage it was restored by solid grafts containing granule but not CA1 pyramidal cells. Furthermore, electrophysiological evidence has demonstrated functional, graft type-specific host-graft functional neuronal connectivity. Thus, restoration of cognitive function by neural transplants is possible after damage to either diffuse (cholinergic) or point-to-point (intrahippocampal) forebrain systems, but the transplant must be appropriate to the damage to be repaired. Because the different types of brain damage studied provide analogues of human alcoholic dementia, Alzheimer's disease, and heart attack, these results are encouraging with regard to the eventual application of neural transplant surgery to the treatment of cognitive deficits in humans.