Disengaging the negative priming mechanism in location tasks

In a location-based negative priming task, targets that appear at locations that were previously occupied by distractors are typically responded to more slowly than are targets that appear at formerly unoccupied positions. In the present study, we attempted to disengage the location-based negative priming mechanism by presenting visual cues indicating the most likely location of the upcoming target. The first experiment showed that 75% cue-target validity was not sufficient to affect the negative priming mechanism. However, the second experiment demonstrated that a much reduced, but not eliminated, negative priming effect occurred with 100%cue-target validity. These findings are similar to those found with inhibition of return, suggesting that location-based inhibition of return effects and location-based negative priming effects may share a common inhibition mechanism.     

Comprehension and production of body part labels in 2‐ to 3‐year‐old children

This study examined which body part labels children could (i) produce when the experimenter touched different locations on her own body, asking each time ‘What's this?’ and (ii) comprehend by touching the correct locations on their own bodies in response to the experimenter asking ‘Where's the [body‐part label]?’. Seventeen children aged between 26 and 41 months, tested in a repeated measures procedure, were presented with 50 different body part stimuli in 200 test trials per child. Overall, the children produced fewer body part labels than they could comprehend. The accuracy of children's responses depended on (i) the location or extent of each body part (facial and broad body features were better known; joints and features in or attached to broad body parts the least well known); (ii) the amount of sensory (but not motor) representation each body part has in the human cortex; and (iii) whether a body part was commonly named by caregivers. These results present a precise mapping of the body parts that young children are able to name and locate on their own bodies in response to body part names; they suggest several possible determinants of lexical‐semantic body knowledge and add to the understanding of how it develops in childhood.     

Differentiating corporal punishment from physical abuse in the prediction of lifetime aggression

Corporal punishment and parental physical abuse often co‐occur during upbringing, making it difficult to differentiate their selective impacts on psychological functioning. Associations between corporal punishment and a number of lifetime aggression indicators were examined in this study after efforts to control the potential influence of various forms of co‐occurring maltreatment (parental physical abuse, childhood sexual abuse, sibling abuse, peer bullying, and observed parental violence). College students (N = 1,136) provided retrospective self‐reports regarding their history of aggression and levels of exposure to childhood corporal punishment and maltreatment experiences. Analyses focused on three hypotheses: 1) The odds of experiencing childhood physical abuse would be higher among respondents reporting frequent corporal punishment during upbringing; 2) Corporal punishment scores would predict the criterion aggression indices after control of variance associated with childhood maltreatment; 3) Aggression scores would be higher among respondents classified in the moderate and elevated corporal punishment risk groups. Strong support was found for the first hypothesis since the odds of childhood physical abuse recollections were higher (OR = 65.3) among respondents who experienced frequent (>60 total disciplinary acts) corporal punishment during upbringing. Partial support was found for the second and third hypotheses. Dimensional and categorical corporal punishment scores were associated significantly with half of the criterion measures. These findings support efforts to dissuade reliance on corporal punishment to manage child behavior.

     

Individual differences in insular sensitivity during loss anticipation predict avoidance learning

The anterior insula has been implicated in both the experience and the anticipation of negative outcomes. Although individual differences in insular sensitivity have been associated with self-report measures of chronic anxiety, previous research has not examined whether individual differences in insular sensitivity predict learning to avoid aversive stimuli. In the present study, insular sensitivity was assessed as participants anticipated monetary losses while undergoing functional magnetic resonance imaging. We found that insular responsiveness to anticipated losses predicted participants' ability to learn to avoid losses (but not to approach gains) in a behavioral test several months later. These findings suggest that in addition to correlating with self-reported anxiety, heightened insular sensitivity may promote learning to avoid loss.     

Working memory deficits in transgenic rats overexpressing human adenosine A2A receptors in the brain

Adenosine receptors in the central nervous system have been implicated in the modulation of different behavioural patterns and cognitive functions although the specific role of A(2A) receptor (A(2A)R) subtype in learning and memory is still unclear. In the present work we establish a novel transgenic rat strain, TGR(NSEhA2A), overexpressing adenosine A(2A)Rs mainly in the cerebral cortex, the hippocampal formation, and the cerebellum. Thereafter, we explore the relevance of this A(2A)Rs overexpression for learning and memory function. Animals were behaviourally assessed in several learning and memory tasks (6-arms radial tunnel maze, T-maze, object recognition, and several Morris water maze paradigms) and other tests for spontaneous motor activity (open field, hexagonal tunnel maze) and anxiety (plus maze) as modification of these behaviours may interfere with the assessment of cognitive function. Neither motor performance and emotional/anxious-like behaviours were altered by overexpression of A(2A)Rs. TGR(NSEhA2A) showed normal hippocampal-dependent learning of spatial reference memory. However, they presented working memory deficits as detected by performance of constant errors in the blind arms of the 6 arm radial tunnel maze, reduced recognition of a novel object and a lack of learning improvement over four trials on the same day which was not observed over consecutive days in a repeated acquisition paradigm in the Morris water maze. Given the interdependence between adenosinic and dopaminergic function, the present results render the novel TGR(NSEhA2A) as a putative animal model for the working memory deficits and cognitive disruptions related to overstimulation of cortical A(2A)Rs or to dopaminergic prefrontal dysfunction as seen in schizophrenic or Parkinson's disease patients.