Correlational cuing as a function of target complexity and target-flanker similarity

It is generally assumed that the correlational cuing effect (CE) between targets and correlated flankers is due to learning association between the flankers and their correlated responses. The present study challenges this view. Experiment 1 shows that the CE for targets composed of color is eliminated as soon as the correlation is removed. Experiment 2 shows that the CE during training is not due to association of the flankers with responses. Experiment 3 shows that at least some of the CE during training with the correlation is due to repetition priming of the display. Experiment 4 replicates the results of Experiment 1 for orientation targets. In Experiments 5-7, more typical tasks with letter targets are examined, and it is demonstrated that preexperimental similarity between targets and correlated flankers is crucial. The CE for correlated but dissimilar target-flanker pairs, similar to that for color and orientation targets, is confined to on-line processes that occur during training. The CE is transferred, however, for correlated and similar target-flanker pairs. We propose that, at least for the simple stimulus to response mapping used in our study, the CE is not due to learning at all. Instead it is due to (1) on-line processes, such as repetition priming, that occur during training with the correlation and (2) a regular flanker effect (see, e.g., B. A. Eriksen & C. W. Eriksen, 1974) that occurs for similar target-flanker pairs.     

Reduction in rat phosphatidylethanolamine binding protein-1 (PEBP1) after chronic corticosterone treatment may be paralleled by cognitive impairment: a first study

Chronic stress is associated with hippocampal atrophy and cognitive dysfunction. This study investigates how long-lasting administration of corticosterone as a mimic of experimentally induced stress affects psychometric performance and the expression of the phosphatidylethanolamine binding protein (PEBP1) in the adult hippocampus of one-year-old male rats. Psychometric investigations were conducted in rats before and after corticosterone treatment using a holeboard test system. Rats were randomly attributed to 2 groups (n = 7) for daily subcutaneous injection of either 26.8 mg/kg body weight corticosterone or sesame oil (vehicle control). Treatment was continued for 60 days, followed by cognitive retesting in the holeboard system. For protein analysis, the hippocampal proteome was separated by 2D electrophoresis (2DE) followed by image processing, statistical analysis, protein identification via peptide mass fingerprinting and gel matching and subsequent functional network mapping and molecular pathway analysis. Differential expression of PEBP1 was additionally quantified by Western blot analysis. Results show that chronic corticosterone significantly decreased rat hippocampal PEBP1 expression and induced a working and reference memory dysfunction. From this, we derive the preliminary hypothesis that PEBP1 may be a novel molecular mediator influencing cognitive integrity during chronic corticosterone exposure in rat hippocampus.     

NK(3) receptor agonism promotes episodic-like memory in mice

The mammalian tachykinins are a family of closely related peptides including substance P, neurokinin A, neurokinin B and, recently, also hemokinin-1. They are present in the peripheral and central nervous systems, and bind to three known neurokinin (NK) receptors, the NK(1)-, NK(2)- and NK(3) receptors. In both rodents and humans, NK(3) receptors are expressed in brain structures which have been associated with learning and memory. Evidence for a role of NK(3) receptors in learning and memory has been found in NK(3) receptor knockout mice. Here, we investigated the influence of the NK(3) receptor agonist, senktide (0.1, 0.2 and 0.4 mg/kg), on the performance of C57BL/6 mice in a recently developed episodic-like memory task. Since a promnestic effect of senktide was expected, we employed an experimental protocol that provided sub-optimal learning conditions for episodic-like memory. The results indicate that senktide promotes episodic-like memory in mice in a dose-dependent manner, providing, for the first time, evidence for an involvement of NK(3) receptors in episodic-like memory.     

When cognitive scientists become religious, science is in trouble: On neurotheology from a philosophy of science perspective

Since the 1990s medical technology has afforded exciting possibilities for studying the brain. Together with knowledge accrued through psychology and psychiatry, it has set the stage for pioneering research and stimulated disciplines such as Social Neuroscience, the Cognitive Science of Religion, Cognitive Anthropology, and Cognitive Archaeology. Another discipline has arisen, Neurotheology, which is interested in the brain and religious experience. Early proponents such as d'Aquili and Newberg had a religious agenda in their work. Others, such as members of Transcendental Meditation, have used experimental and brain studies to legitimate religious agendas. Experiential shamanists have embarked on a similar legitimation process. The differences between science and therapy and spirituality have been blurred or denied. Neurotheological attempts to discover areas of the brain responsible for religious experiences have led to untenable results. The fact that such research has passed the peer review process of leading psychological, psychiatric, and neurological journals is perhaps more indicative of the pervasiveness of religiosity throughout American society than of objective brain science. This essay argues that neurotheology is an example of the struggle between confessional and critical approaches to the study of religion. The main difference is that the battlefield of this struggle is the brain.     

The association between life events and suicide intent in self-poisoners with and without a history of deliberate self-harm: a preliminary study

The associations between life events in the 12 months preceding an episode of self-poisoning resulting in hospital attendance (the index episode), and the suicide intent of this episode were compared in individuals for whom the index episode was their first, episode and in individuals in whom it was a recurrence of DSH. Results indicated a significant interaction between independent life events, repetition status, and gender in the prediction of suicide intent, the association between life events and intent being moderated by repetition status in women only. The results provide preliminary evidence to suggest the presence of a suicidal process in women, in which the impact of negative life events on suicide intent diminishes across episodes.     

Does any aspect of mind survive brain damage that typically leads to a persistent vegetative state? Ethical considerations

Recent neuroscientific evidence brings into question the conclusion that all aspects of consciousness are gone in patients who have descended into a persistent vegetative state (PVS). Here we summarize the evidence from human brain imaging as well as neurological damage in animals and humans suggesting that some form of consciousness can survive brain damage that commonly causes PVS. We also raise the issue that neuroscientific evidence indicates that raw emotional feelings (primary-process affects) can exist without any cognitive awareness of those feelings. Likewise, the basic brain mechanisms for thirst and hunger exist in brain regions typically not damaged by PVS. If affective feelings can exist without cognitive awareness of those feelings, then it is possible that the instinctual emotional actions and pain "reflexes" often exhibited by PVS patients may indicate some level of mentality remaining in PVS patients. Indeed, it is possible such raw affective feelings are intensified when PVS patients are removed from life-supports. They may still experience a variety of primary-process affective states that could constitute forms of suffering. If so, withdrawal of life-support may violate the principle of nonmaleficence and be tantamount to inflicting inadvertent "cruel and unusual punishment" on patients whose potential distress, during the process of dying, needs to be considered in ethical decision-making about how such individuals should be treated, especially when their lives are ended by termination of life-supports. Medical wisdom may dictate the use of more rapid pharmacological forms of euthanasia that minimize distress than the de facto euthanasia of life-support termination that may lead to excruciating feelings of pure thirst and other negative affective feelings in the absence of any reflective awareness.     

Criticizing groups from the inside and the outside: an identity perspective on the intergroup sensitivity effect

Research on group criticism has demonstrated that criticisms are received less defensively when made by an ingroup member than when made by an outsider (the intergroup sensitivity effect). Three experiments tested the extent to which this effect is driven by social identity concerns or by judgments of how experienced the source of the criticism is. In Experiments 1 and 2, Australians who criticized Australia (ingroup critics) were met with less defensiveness than were foreigners who criticized Australia (outgroup critics), regardless of the amount of experience the foreigner had with Australia. Furthermore, the effects of speaker type on evaluations were mediated by perceptions of the extent to which the criticisms were intended to be constructive but not by perceptions of experience. Finally, Experiment 3 indicated that although experience does not help outgroup critics, a lack of experience can hurt ingroup critics. Recommendations are provided as to how people can reduce defensiveness when making group criticisms.     

A short history of ideo-motor action

The ideo-motor theory, which is currently receiving heightened interest in cognitive psychology, looks back on a long history. Essentially two historical roots can be presented. A British one, initiated by Laycock (1845) and Carpenter (1852), which was developed in order to explain ideo-motor phenomena by means of cerebral reflex actions. A second and older root is the German one by Herbart (1816, 1825), Lotze (1852), and Harless (1861), which considered the ideo-motor principle a fundamental mechanism of all intentional human behaviour. Both roots converged in James' (1890) Principles of Psychology before they fell into oblivion due to the dominance of behaviorism in the first half of the 20th century. The few empirical ideo-motor studies of the early 20th century are briefly described. Finally, similarities and differences in the history of the ideo-motor theory are delineated and a perspective is given covering research questions that could be examined in the future.     

Influence of chronic corticosterone and glucocorticoid receptor antagonism in the amygdala on fear conditioning

Glucocorticoid receptor activation within the basolateral amygdala (BLA) during fear conditioning may mediate enhancement in rats chronically exposed to stress levels of corticosterone. Male Sprague-Dawley rats received corticosterone (400 microg/ml) in their drinking water (days 1-21), a manipulation that was previously shown to cause hippocampal CA3 dendritic retraction. Subsequently, rats were adapted to the fear conditioning chamber (day 22), then trained (day 23), and tested for conditioned fear to context and tone (day 25). Training consisted of two tone (20s) and footshock (500 ms, 0.25 mA) pairings. In Experiment 1, muscimol (4.4 nmol/0.5 microl/side), a GABAergic agonist, was microinfused to temporarily inactivate the BLA during training. Rats given chronic corticosterone showed enhanced freezing to context, but not tone, compared to vehicle-supplemented rats. Moreover, BLA inactivation impaired contextual and tone conditioning, regardless of corticosterone treatment. In Experiment 2, RU486 (0, 0.3, and 3.0 ng/0.2 microl/side) was infused on training day to antagonize glucocorticoid receptors in the BLA. Corticosterone treatment enhanced fear conditioning to context and tone when analyzed together, but not separately. Moreover, RU486 (3.0 ng/side) selectively exacerbated freezing to context in chronic corticosterone-exposed rats only, but failed to alter tone conditioning. Serum corticosterone levels were negatively correlated with contextual, not tone, conditioning. Altogether, these suggest that chronic corticosterone influences fear conditioning differently than chronic stress as shown previously. Moreover, chronic exposure to corticosteroids alters BLA functioning in a non-linear fashion and that contextual conditioning is influenced more than tone conditioning by chronic corticosterone and BLA glucocorticoid receptor stimulation.     

Social stress in tree shrews as an animal model of depression: an example of a behavioral model of a CNS disorder

Animal models are invaluable in preclinical research on human psychopathology. Valid animal models to study the pathophysiology of depression and specific biological and behavioral responses to antidepressant drug treatments are of prime interest. In order to improve our knowledge of the causal mechanisms of stress-related disorders such as depression, we need animal models that mirror the situation seen in patients. One promising model is the chronic psychosocial stress paradigm in male tree shrews. Coexistence of two males in visual and olfactory contact leads to a stable dominant/subordinate relationship, with the subordinates showing obvious changes in behavioral, neuroendocrine, and central nervous activity that are similar to the signs and symptoms observed during episodes of depression in patients. To discover whether this model, besides its "face validity" for depression, also has "predictive validity," we treated subordinate animals with the tricyclic antidepressant clomipramine and found a time-dependent recovery of both endocrine function and normal behavior. In contrast, the anxiolytic diazepam was ineffective. Chronic psychosocial stress in male tree shrews significantly decreased hippocampal volume and the proliferation rate of the granule precursor cells in the dentate gyrus. These stress-induced changes can be prevented by treating the animals with clomipramine, tianeptine, or the selective neurokinin receptor antagonist L-760,735. In addition to its apparent face and predictive validity, the tree shrew model also has a "molecular validity" due to the degradation routes of psychotropic compounds and gene sequences of receptors are very similar to those in humans. Although further research is required to validate this model fully, it provides an adequate and interesting non-rodent experimental paradigm for preclinical research on depression.