Variation in cue duration reveals top-down modulation of involuntary orienting to uninformative symbolic cues

This article reports three experiments in which the effects of cue duration on involuntary orienting to uninformative symbolic cues (arrows presented at fixation) were investigated. Experiment 1 showed that symbolic cues had less effect on involuntary orienting when they were presented for only 25 msec than when they were presented for 200 msec across a range of stimulus onset asynchronies. Experiment 2 suggested that the effect of cue duration on involuntary orienting was due primarily to top-down strategic factors, rather than to bottom-up stimulus factors, and Experiment 3 suggested that these strategic factors may involve differences in how the cue is processed. Altogether, the present findings are important because they emphasize the distinction between cue processing and the putative involuntary orienting that results from such processing in the symbolic-cuing paradigm. In so doing, the present results help resolve discrepant findings that have been reported across previous studies.     

Effects of sex on raters' accountability

The effects of sex (rater and ratee) on raters' accountability in the context of performance appraisal were investigated. The 130 participating undergraduates (men and women) rated a fictitious male or female's performance on a clerical task subsequent to receiving self-assessment information. As expected, raters' knowledge of a high self-assessment was followed by significantly higher performance ratings than after knowledge of a low self-assessment. Contrary to expectations, no differences were found for either raters' or ratees' sex. The results suggest that the sex of the rater or ratee is not associated with raters' accountability.     

Chronically increased Gsalpha signaling disrupts associative and spatial learning

The cAMP/PKA pathway plays a critical role in learning and memory systems in animals ranging from mice to Drosophila to Aplysia. Studies of olfactory learning in Drosophila suggest that altered expression of either positive or negative regulators of the cAMP/PKA signaling pathway beyond a certain optimum range may be deleterious. Here we provide genetic evidence of the behavioral and physiological effects of increased signaling through the cAMP/PKA pathway in mice. We have generated transgenic mice in which the expression of a constitutively active form of Gsalpha (Gsalpha* Q227L), the G protein that stimulates adenylyl cyclase activity, is driven in neurons within the forebrain by the promoter from the CaMKIIalpha gene. Despite significantly increased adenylyl cyclase activity, Gsalpha* transgenic mice exhibit PKA-dependent decreases in levels of cAMP due to a compensatory up-regulation in phosphodiesterase activity. Interestingly, Gsalpha* transgenic mice also exhibit enhanced basal synaptic transmission. Consistent with a role for the cAMP/PKA pathway in learning and memory, Gsalpha* transgenic mice show impairments in spatial learning in the Morris water maze and in contextual and cued fear conditioning tasks. The learning deficits observed in these transgenic mice suggest that associative and spatial learning requires regulated Gsalpha protein signaling, much as does olfactory learning in Drosophila.     

Behavioral Family Interventions for Improving Child-rearing: A Review of the Literature for Clinicians and Policy Makers

This paper reviews evidence that behavioral family interventions are effective at improving child-rearing in distressed families and families with children exhibiting disruptive behavior. Essential therapeutic strategies offered within a collaborative therapeutic process are identified. Exemplary materials for parents and clinicians are identified. Differences between behavioral family interventions and two popular press parenting approaches are highlighted, including the lack of empirical support for these widely used programs and the advice they offer which runs counter to behavioral approaches. Recommendations are offered for combining behavioral family interventions with other empirically supported approaches, promoting more widespread use of empirically supported treatments, such as behavioral family interventions, and the need for a public health perspective on family functioning, involving collaboration among clinicians, policy makers, and researchers.     

DENTIST-IMPLEMENTED CONTINGENT ESCAPE FOR MANAGEMENT OF DISRUPTIVE CHILD BEHAVIOR

We evaluated the effectiveness of a dentist-implemented intervention in which brief escape from dental treatment was provided to manage disruptive child behavior during restorative dental treatment. Within a multiple baseline design across subjects, 4 children, aged 3 to 7 years, were provided temporary escape from dental treatment contingent upon brief periods of cooperative behavior. Disruptive behavior decreased when the appropriate escape contingency was used at least 80% of the time. The escape contingency required no more time than traditional management procedures (e.g., tell-show-do, reprimands and loud commands, restraint) to bring disruptive behavior under control. Independent ratings by two dentists provided social validation of the efficacy of the escape contingency.     

Happiness and health: environmental and genetic contributions to the relationship between subjective well-being, perceived health, and somatic illness

The aim was to identify genetic and environmental influences on the covariances between subjective well-being (SWB), perceived health, and somatic illness. Analyses were based on 6576 Norwegian twins aged 18-31. Heritabilities ranged from .24 to.66. SWB correlated .50 with perceived health, -.25 with musculoskeletal pain, and -.07 with allergy. Common genetic factors accounted for 45%-60% of associations. SWB and perceived health was to a high extent influenced by the same genes (r(g)=.72 and.82 for males and females, respectively). For SWB and musculoskeletal pain, r-sub(g) =-.29 and -.42 for males and females, respectively. Effects were partly sex specific. Environmental factors shared by twins did not affect the covariances. Results support a differentiated view of SWB-health relations, and imply that both genes and environment play important roles in the associations between well-being and health.     

Constitutive activation of the G-protein subunit Galphas within forebrain neurons causes PKA-dependent alterations in fear conditioning and cortical Arc mRNA expression

Memory formation requires cAMP signaling; thus, this cascade has been of great interest in the search for cognitive enhancers. Given that medications are administered long-term, we determined the effects of chronically increasing cAMP synthesis in the brain by expressing a constitutively active isoform of the G-protein subunit Galphas (Galphas*) in postnatal forebrain neurons of mice. Previously, we showed that Galphas* mice exhibit increased adenylyl cyclase activity but decreased cAMP levels in cortex and hippocampus due to a PKA-dependent increase in total cAMP phosphodiesterase (PDE) activity. Here, we extend previous findings by determining if Galphas* mice show increased activity of specific PDE families that are regulated by PKA, if Galphas* mice show PKA-dependent deficits in fear memory, and if these memory deficits are associated with PKA-dependent alterations in neuronal activity as mapped by Arc mRNA expression. Consistent with previous findings, we show here that Galphas* mice exhibit a significant compensatory increase in cAMP PDE1 activity and a trend toward increased cAMP PDE4 activity. Further, inhibiting the presumably elevated PKA activity in Galphas* mice fully rescues short- and long-term memory deficits in a fear-conditioning task, while extending the training session from one to four CS-US pairings partially rescues these deficits. Mapping of Arc mRNA levels suggests these PKA-dependent memory deficits may be related to decreased neuronal activity specifically within the cortex. Galphas* mice show decreased Arc mRNA expression in CA1, orbital cortex, and cortical regions surrounding the hippocampus; however, only the deficits in cortical regions surrounding the hippocampus are PKA dependent. Our results imply that chronically stimulating targets upstream of cAMP may detrimentally affect cognition.