in addition to endogenously produced opiates, which are part of normal affiliative neurocircuitry and attachment formation, exogenous opiates – such as drugs of addiction and abuse – may affect affiliation. we consider possible modulatory effects of such exogenous opiates on the development of early parent–infant attachment from both parents' and infants' perspectives.

brain opioids regulate social emotions in several distinct ways. the abundance of neuroscientific detail in the target article helps familiarize the uninitiated with the true and humbling complexities of mammalian brains, but little of it translates to research strategies, with robust predictions, at the human level. only global neurochemical affective state variables derived from animal research have clear implications for human research.

in sagvolden et al.'s conceptualization of how a poor behavioral, social, and academic repertoire arises from an impaired interaction with the environment of an individual with a neurological disorder, we see a convergence between the medical diagnosis and the functional assessment on which the behavioral educational approach is based. if children with such a disorder do show delay-of-reinforcement steepened gradients, it is possible to predict their behavior under given circumstances. this could bring us to more precise diagnostic criteria and better intervention techniques.

the dynamic developmental theory of attention-deficit/hyperactivity disorder (adhd) proposes that hypodopaminergic functioning results in anomalous delay-of-reinforcement gradients in adhd, which in turn might account for many of the observed behavioral and cognitive characteristics. however, hyperdopaminergic functioning might also impair mnemonic representation of codes for spatial, motoric, and reward information and contribute to the purported shorter delay gradients in adhd.

“a dynamic developmental theory of attention-deficit/hyperactivity disorder (adhd) predominantly hyperactive/impulsive and combined subtypes” is a major contribution linking comparative psychology with clinical developmental neuropsychopathology. in this commentary, i place some critical remarks concerning the theory's explanation of sleep problems, inhibition, error monitoring, and motor control.

affect mirroring allows infants to distinguish emotional and intentional states of significant others, which – in the pursuit of their own drive satisfaction, including satisfaction of the affiliative drive – become important contextual stimuli predictive of reward. learning to perceive and manipulate others' attitudes toward oneself in pursuit of affiliative reward may be an important step in social development that is impaired in autism.

notwithstanding the many strengths of the dynamic developmental theory, there remain challenges to be overcome before it can be incorporated into a true causal model of attention-deficit/hyperactivity disorder (adhd). these include the development of reliable measures of reinforcement delay gradients, the validation of shortened reinforcement delay as an endophenotype, and the integration of this pathway with other potential pathways.

despite general agreement that altered reward sensitivity is involved in attention-deficit/hyperactivity disorder (adhd), a wide range of different alterations has been proposed. we cite work showing abnormal sensitivity to delay of reward, together with abnormal sensitivity to individual instances of reward. we argue that at the cellular level these behavioural characteristics might indicate that dopamine timing is off in children with adhd.

Miller and Rodgers (2001) proposed a central nervous system based Ontogenetic Bonding System that operates across the life course to promote succorant, 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.

commentary on our target article centers around six main topics: (1) strategies in modeling the neurobehavioral foundation of human behavioral traits; (2) clarification of the construct of affiliation; (3) developmental aspects of affiliative bonding; (4) modeling disorders of affiliative reward; (5) serotonin and affiliative behavior; and (6) neural considerations. after an initial important research update in section r1, our response is organized around these topics in the following six sections, r2 to r7.

early and automatic neuropsychological processes may be influenced by altered dopaminergic functions but cannot be fully explained by these or by altered reinforcement and extinction processes. the reinforcement-extinction model is excellent for understanding certain causal pathways of attention-deficit/hyperactivity disorder (adhd), but it can hardly explain the heterogeneous developmental trajectories of adhd fully. it should be integrated into a multiple pathways model.

primate research suggests that affiliation is a highly complex construct. studies of primate affiliation demonstrate the need to distinguish between various affiliative behaviors, consider relationships as emergent properties of these behaviors, define affiliation in the context of general environmental responsiveness, and address developmental changes in affiliation across the lifespan.

in the target article, sagvolden and collaborators propose that attentional-deficit/hyperactivity disorder (adhd) is the result of a general behavioral deficit which is mainly caused by a hypofunctioning mesolimbic dopaminergic system. although we partly agree with this view, we think that it tends to overlook the dysfunction of prefrontal and frontostriatal executive functions by considering them to be a consequence of alterations in reward and extinction mechanisms. rather, we believe that adhd is the result of an overall cognitive and behavioral condition, associated to a generalized dopaminergic network dysfunction, and may not be easily attributable to a single basic behavioral function.

the possible role of the neurotransmitter serotonin in human affiliative behavior is under-examined in the review by depue & morrone-strupinsky (d&m-s). this commentary reviews evidence indicating that serotonin not only inhibits aggressive behavior that may be detrimental to affiliative bonds with others in a social group but serotonin also enhances prosocial behaviors that may facilitate ties to the social group.

decay gradients are usually drawn facing the wrong direction. righting them emphasizes the role of stimuli that mark the response, and leads to different inferences concerning the factors controlling response–reinforcer associations. a simple model of the concatenation of stimulus traces provides some insight to the problems of impulse control relevant to adhd.

sagvolden, johansen, aase, and russell (sagvolden et al.) examine attention-deficit/hyperactivity disorder (adhd) at levels of analysis ranging from neurotransmitters to behavior. at the behavioral level they attribute aspects of adhd to anomalies of delay-of-reinforcement gradients. with a normal gradient, responses followed after a long delay by a reinforcer may share in the effects of that reinforcer; with a diminished or steepened gradient they may fail to do so. steepened gradients differentially select rapidly emitted responses (hyperactivity), and they limit the effectiveness with which extended stimuli become conditioned reinforcers, so that observing behavior is less well maintained (attention deficit). impulsiveness also follows from steepened gradients, which increase the effectiveness of smaller, more immediate consequences relative to larger, more delayed ones. individuals who vary in the degree to which their delay gradients are steepened will show different balances between hyperactivity and attention deficit. given the range of adhd phenomena addressed, it may be unnecessary to appeal to additional behavioral processes such as extinction deficit. extinction deficit is more likely a derivative of attention deficit, in that failure to attend to stimuli differentially correlated with extinction should slow its progress. the account suggests how relatively small differences in delay gradients early in development might engender behavioral interactions leading to very large differences later on. the steepened gradients presumably originate in properties of neurotransmitter function, but behavioral interventions that use consistently short delays of reinforcement to build higher-order behavioral units as a scaffolding to support complex cognitive and social skills may nonetheless be feasible.

the reinforcement/extinction disorder hypothesis (sagvolden et al.) is an important counterweight to the executive dysfunction model of attention-deficit/hyperactivity disorder (adhd). however, like that model, it conceptualises adhd as pathophysiologically homogeneous, resulting from a common core dysfunction. recent studies reporting neuropsychological heterogeneity suggest that this common core dysfunction may be the scientific equivalent of a red herring.

depue & morrone-strupinsky's (d&m-s's) language suggests that, unlike kent berridge, they may allow that the activity of a largely subcortical system, which is presumably often introspectively and cognitively inaccessible, constitutes affectively felt experience even when so. such experience would then be phenomenally conscious without being reflexively conscious or cognitively access-conscious, to use distinctions formulated by the philosopher ned block.

both the target article and the precommentary demonstrate that relatively simple biobehavioral processes have the cumulative effect of fostering behavioral outcomes characteristic of attention-deficit/hyperactivity disorder (adhd). as such, the articles illustrate a central theme of darwinian thinking – basic processes acting over time can produce complex and diverse outcomes. in this commentary, we indicate that tracing the action of processes over time can be facilitated by quantitative methods such as artificial neural networks.

the authors regard opiates as the primary neural substrate for social attachment, and peptide hormones as subsidiary. one may instead conclude from their evidence that oxytocin, vasopressin, and opiates play complementary roles in attachment. oxytocin and vasopressin relate to different aspects of emotional experience, and opiates to quiescence from long-term attachment. this is related to intimacy versus affiliation.