A number of models developed in the adult psychopathology literature (i.e., L. A. Clark & D. Watson, 1991) have asserted that low levels of positive emotionality (PE) are predisposing factors or precursors for depression and represent a form of temperamental risk for depression. Further support for this claim would derive from evidence linking low PE to known indicators of risk for depression. The authors examined the association between temperamental emotionality in young children and parental mood disorders. One hundred unselected preschool-aged children completed a battery of emotion-eliciting tasks tapping aspects of PE, negative emotionality (NE), and behavioral inhibition (BI). Parental psychopathology was assessed with semistructured diagnostic interviews. Low PE in children was associated with maternal, but not paternal, mood disorder. The low PE-maternal depression link was relatively specific, as there were few associations between low PE and other forms of parental psychopathology or between NE and BI and parental mood disorders.

A key component of temperament models is the presumed temporal stability of temperament traits. Although a substantial literature using parent report measures has addressed this claim, very few investigations have examined the stability of temperament using alternative measurement strategies, particularly those that involve direct assessment of emotional expressions. This study reports on the relative stability and heterotypic continuity of temperament traits measured via laboratory tasks and maternal report in a sample of children assessed at ages 3, 5, and 7, focusing on Positive Emotionality and Negative Emotionality. Relative stability of Positive Emotionality and Negative Emotionality traits ranged from moderate to high for laboratory and maternal report measures. Measures of emotional expressions exhibited levels of stability comparable to or higher than traits defined by other behavioral patterns (e.g., sociability and engagement).

for help with data collection. Thanks also to the families who participated in this study. This work was supported by NIMH grants RO1 MH069942 (DNK) and f31 MH075484-01A2 (LRD).

Carver and White's Behavioral Inhibition System/Behavioral Activation System (BIS/BAS) Scale has been a useful tool for studying individual differences in reward/punishment sensitivity; however, its factor structure and invariance across development have not been well tested. In the current study, we examined the factor structure of the BIS/BAS Scale across five age groups: 6-10-year-old children (N=229), 11-13-year-old early adolescents (N=311), 14-16-year-old late adolescents (N=353), 18-22-year-old young adults (N=844), and 30-45-year-old adults (N=471). Given poor fit of the standard four-factor model (BIS, Reward Responsivity, Drive, Fun Seeking) in the literature, we conducted exploratory factor analyses in half of the participants and identified problematic items across age groups. The four-factor model showed poor fit in our sample whereas removing the BAS Fun Seeking subscale and problematic items from the remaining subscales improved fit in confirmatory factor analyses conducted with the second half of the participants. The revised model showed strict invariance across age groups and by sex, indicating consistent factor structure, item loadings, thresholds, and unique/residual variances. Additionally, in our cross-sectional data, we observed non-linear relations between age and subscale scores, where scores tended to be higher in young adulthood than childhood and later adulthood. Furthermore, sex differences emerged across development; adolescent and adult females had higher BIS scores than males in this age range, whereas sex differences were not observed in childhood. These differences may help us to understand the rise in internalizing psychopathology in adolescence, particularly in females. Future developmental studies are warranted to examine the impact of rewording problematic items.

We describe a comprehensive translational approach for identifying candidate genes for alcoholism. The approach relies on the cross-matching of animal model brain gene expression data with human genetic linkage data, as well as human tissue data and biological roles data, an approach termed convergent functional genomics. An analysis of three animal model paradigms, based on inbred alcohol-preferring (iP) and alcohol-non-preferring (iNP) rats, and their response to treatments with alcohol, was used. A comprehensive analysis of microarray gene expression data from five key brain regions (frontal cortex, amygdala, caudate-putamen, nucleus accumbens and hippocampus) was carried out. The Bayesian-like integration of multiple independent lines of evidence, each by itself lacking sufficient discriminatory power, led to the identification of high probability candidate genes, pathways and mechanisms for alcoholism. These data reveal that alcohol has pleiotropic effects on multiple systems, which may explain the diverse neuropsychiatric and medical pathology in alcoholism. Some of the pathways identified suggest avenues for pharmacotherapy of alcoholism with existing agents, such as angiotensin-converting enzyme (ACE) inhibitors. Experiments we carried out in alcohol-preferring rats with an ACE inhibitor show a marked modulation of alcohol intake. Other pathways are new potential targets for drug development. The emergent overall picture is that physical and physiological robustness may permit alcohol-preferring individuals to withstand the aversive effects of alcohol. In conjunction with a higher reactivity to its rewarding effects, they may able to ingest enough of this nonspecific drug for a strong hedonic and addictive effect to occur.