Extraversion has two central characteristics: (1) interpersonal engagement, which consists of affiliation (enjoying and valuing close interpersonal bonds, being warm and affectionate) and agency (being socially dominant, enjoying leadership roles, being assertive, being exhibitionistic, and having a sense of potency in accomplishing goals) and (2) impulsivity, which emerges from the interaction of extraversion and a second, independent trait (constraint). Agency is a more general motivational disposition that includes dominance, ambition, mastery, efficacy, and achievement. Positive affect (a combination of positive feelings and motivation) is closely associated with extraversion. Extraversion is accordingly based on positive incentive motivation.Parallels between extraversion (particularly its agency component) and a mammalian behavioral approach system based on positive incentive motivation implicate a neuroanatomical network and modulatory neurotransmitters in the processing of incentive motivation. A corticolimbic-striatal-thalamic network (1) integrates the salient incentive context in the medial orbital cortex, amygdala, and hippocampus; (2) encodes the intensity of incentive stimuli in a motive circuit composed of the nucleus accumbens, ventral pallidum, and ventral tegmental area dopamine projection system; and (3) creates an incentive motivational state that can be transmitted to the motor system.Individual differences in the functioning of this network arise from functional variation in the ventral tegmental area dopamine projections, which are directly involved in coding the intensity of incentive motivation. The animal evidence suggests that there are three neurodevelopmental sources of individual differences in dopamine: genetic, “experience-expectant,” and “experience-dependent.” Individual differences in dopamine promote variation in the heterosynaptic plasticity that enhances the connection between incentive context and incentive motivation and behavior.Our psychobiological threshold model explains the effects of individual differences in dopamine transmission on behavior, and their relation to personality traits is discussed.

Because little is known about the human trait of affiliation, we provide a novel neurobehavioral model of affiliative bonding. Discussion is organized around processes of reward and memory formation that occur during approach and consummatory phases of affiliation. Appetitive and consummatory reward processes are mediated independently by the activity of the ventral tegmental area (VTA) dopamine (DA)-nucleus accumbens shell (NAS) pathway and the central corticolimbic projections of the u-opiate system of the medial basal arcuate nucleus, respectively, although these two projection systems functionally interact across time. We next explicate the manner in which DA and glutamate interact in both the VTA and NAS to form incentive-encoded contextual memory ensembles that are predictive of reward derived from affiliative objects. Affiliative stimuli, in particular, are incorporated within contextual ensembles predictive of affiliative reward via: (a) the binding of affiliative stimuli in the rostral circuit of the medial extended amygdala and subsequent transmission to the NAS shell; (b) affiliative stimulus-induced opiate potentiation of DA processes in the VTA and NAS; and (c) permissive or facilitatory effects of gonadal steroids, oxytocin (in interaction with DA), and vasopressin on (i) sensory, perceptual, and attentional processing of affiliative stimuli and (ii) formation of social memories. Among these various processes, we propose that the capacity to experience affiliative reward via opiate functioning has a disproportionate weight in determining individual differences in affiliation. We delineate sources of these individual differences, and provide the first human data that support an association between opiate functioning and variation in trait affiliation.

In an attempt to study predisposition to bipolar manic-depressive disorder, we developed a behavioral paradigm to identify persons at risk for various forms of the disorder. We provide a theoretical discussion for denning bipolar disorder within the broader framework of common human diseases and then employ this framework to derive dimensions of bipolar disorder that define its distinctness from the normal phenotype. These dimensions (behavioral and nonbehavioral features of disorder) are operationalized in the form of a self-report inventory which estimates the probability that an individual is at risk. Five external validation studies using nontest criteria are presented, including interview, roommate, family history, clinical characteristics, and longitudinal mood rating investigations. Results indicate that the inventory serves as a promising first-stage case identification procedure for bipolar disorder when employed in a research context. To date, most research on human disorders has focused on the pathophysiology underlying signs and symptoms (Depue & Evans, 1981). If comprehensive models of etiology are to be derived, however, other

Validated the General Behavior Inventory (GBI), revised to identify unipolar as well as bipolar affective conditions, in a nonclinical sample (n = 201) against naive, interview-derived diagnoses. For bipolar and unipolar conditions, respectively, the GBI had high positive (.94, .87) and negative (.99, .93) predictive power with the effect of prevalence considered, adequate sensitivity (.78, .76), high specificity (.99, .99), and adequate selection ratios for sampling of affective and nonaffective subjects from nonclinical populations for research purposes. The utility of the GBI in several different research contexts is discussed.

We use the term disorder for the sake of economy in a very general way to refer to both the general physical and psychological states that are currently assessed in life stress research. This includes general psychological distress and negative affect as well.