previous research into human traits has reached impressive consensus regarding at least some traits, but recent evidence suggests these to be genetically heterogeneous. this is problematic for theories of the neurobiology of human traits. future research should more closely integrate genetic, behavioral, and psychometric research to arrive at biologically validated measurement instruments, which may be better used to understand the mediating role of these traits in the association between genetic variants and complex behaviors.

in this commentary, i argue that the theory presented by sagvolden et al. can be much stronger if its scope is limited, if its developmental aspects are refined, if it can be made to generate testable predictions, and if it can be supported with more data from humans.

depue & morrone-strupinsky's (d&m-s's) model of affiliation meets the criteria advanced for the definition of behavior systems and endophenotypes. we argue that its application in psychiatry could be useful for identifying a biological pathophysiology common to a variety of conditions that are currently classified in very different categories of psychiatric nosography, including autism, schizoid personality, primary psychopathy, and dismissing attachment.

in the present commentary we expand on two concepts relevant to understanding affliliative bonding. differences and similarities between the functions and actions of oxytocin and vasopressin are difficult to study but may be critical to an understanding of mechanisms for social bonding. what is termed here a “trait of affiliation” may reflect in part the capacity of these same peptides to program the developing nervous system.

whether or not trait affiliation correlates with human behaviour needs investigating. one should be careful generalizing neuropsychological mechanisms for affiliation, and generalizing an analysis based on one or two neuropsychological mechanisms and mostly studies on rodents, to complex human social interactions. serotonin is an example of a neurotransmitter playing an important role in cooperation and interacting with the dopaminergic system.

the construct for affiliation in depue & morrone-strupinsky's (d&m-s's) study is restricted to the interpersonal domain. this restriction is not found in other disciplines. it may be necessary in early stages of trait research. but the construct will need to be expanded to speak to the more complex, second-order affiliations of which humans are capable.

miller and rodgers (2001) proposed a central nervous system based ontogenetic bonding system that operates across the life course to promote succorant,“succorance” is a term coined by murray (1938) to describe a general tendency to seek the help and protection of others. affiliative, sexual, and nurturant bonds. i discuss features of this theoretical framework that can inform depue & morrone-strupinsky's (d&m-s's) model. most important, i suggest that the affiliative reward processes d&m-s describe are better conceptualized as subserving the affect/motivation of affection.

the “dynamic developmental” theory of attention-deficit/hyperactivity disorder (adhd) has come full circle from wender's (1971) reinforcement hypothesis. by specifying the principle of time constraints on reinforcement and extinction, the present theory allows for empirical validation. however, the theory implies, but does not discuss, implications for the neurophysiology of comorbidity in adhd. the authors' attribution of comorbid oppositional behavior to parental and societal reinforcement leaves out biological factors.

correcting the relationship between tonic and burst firing modes in dopamine neurons may help normalise stimulus-reinforcement gradients and contingent behaviour in attention-deficit/hyperactivity disorder (adhd) children. but appropriate evaluations of stimuli for developing adaptive plans and controlling impulsivity will not occur without moderating the gain-like functions of serotonin. the “dynamic theory” correctly highlights the need to account for variability in adhd. the dysmaturation of pre-executive information processing is proposed as an explanation.

at the core of the article by sagvolden and colleagues there is a set of data that throws light on an aspect of the adhd phenomenon. but one asks if the authors are a measure too brave to generalise so broadly from the unusually steep reinforcement gradients reported for the human condition and an animal model to the syndrome as a whole.

attention-deficit/hyperactivity disorder (adhd) represents adaptation to defective neurotransmission – an adaptation seldom with benefit. the resulting behavioural style not only increases vulnerability to adverse experiences, but also creates a context in which encountering adversity is more likely. furthermore, the fact that adhd is a highly heritable condition increases the probability of a child with a compromised neurobiological disposition being raised by caregivers with suboptimal resources.

sleep disturbances are common for children with attention-deficit/hyperactivity disorder (adhd) and are of great clinical significance. brain dopamine plays an important role for both adhd symptoms and sleep-wake regulation. we therefore suggest that one basic aspect of integrative brain-behavior relationship such as the sleep-wake cycle may certainly be addressed in a dynamic developmental theory of adhd.

trust is a temporary attachment between humans that pervades our daily lives. recent research has shown that the affiliative hormone oxytocin rises with a social signal of interpersonal trust and is associated with trustworthy behavior (the reciprocation of trust). this commentary reports these results and relates them to the target article's findings for variations in affiliative-related behaviors.

depue & morrone-strupinsky's (d&m-s's) implicit assumption appears to be that affiliative bonding is either strengthened or maintained with time; however, it is more realistic that it can also be weakened or destroyed by conflictive interpersonal interactions. without specifying the mechanisms by which antagonistic stimuli deteriorate affiliative bonding, the model is incapable of accounting for the dynamics associated with this complex phenomenon.

the dynamic developmental theory (ddt) has benefited from the insights of the commentators, particularly in terms of the implications for the proposed steepened delay gradients in attention-deficit/hyperactivity disorder (adhd). the introduction of modified memory processes as a basis for the delay gradients improved the links to aspects of adhd. however, it remains unclear whether the hyperactive-impulsive and inattentive subtypes are separate subgroups or may be explained as different outcomes of the same genetic factors and thus explicable by the same principles. the ddt suggests that altered reinforcement and extinction processes define an endophenotype in adhd that can be related dimensionally to inattention, hyperactivity, and impulsivity. the relation between the suggested endophenotype, characterized by changes in basic learning mechanisms, and other endophenotypes characterized by delay aversion or response disinhibition, needs to be tested in future studies.

support for a neurobiological distinction between affiliation (attachment) and agency (achievement) was achieved by comparing responses to a dopaminergic (da) and a serotonergic (5-ht) challenge test. da responses were similar, but a 5-ht modulation of da emerged for achievement and not for attachment. molecular genetics performed on panksepp's dimension “care” revealed an association with a polymorphism of the da catabolizing enzyme comt that was not associated with separation distress.

research on the neurobiology and psychosocial features of major depressive disorder has the ability to extend our understanding of affiliative behavior. in depression, decreased hedonic capacity and hypoactivity in dopaminergic and prefrontal circuitries may decrease the ability to experience affiliative relationships as rewarding. we suggest that neurobiological research on depression can provide a test case for theoretical models of affiliation.

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.

depue & morrone-strupinsky (d&m-s) have elaborated a detailed description of the motivational system for affiliation and its neurological basis. this “bottom-up” approach, based almost entirely on studies of nonhuman species, fails to connect with personality differences at the human level. a “top-down” approach looks for common biological markers in human and nonhuman species and relates these to behavior in both.

we have shown in a computational model that a poor memory for context could result in some of the behaviors associated with adhd, which is well in line with the dynamic developmental theory. given the important role of context in extinction, a weaker context due to a steeper delay-of-reinforcement gradient would result in impaired inhibition.

major contributions emanating from sagvolden et al.'s theory include elucidation of the role in attention-deficit/hyperactivity disorder (adhd) of temporal information processing, social learning, and response extinction learning. key issues include a need for clearer explanation of the relative role of impulsivity versus response suppression/inhibition in the dual process model, and delineation of genotype-environment correlations versus interactions in the social and experiential mechanisms posited.