To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure email@example.com
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
A dimensional model of personality disturbance is presented that is defined by extreme values on interacting subsets of seven major personality traits. Being at the extreme has marked effects on the threshold for eliciting those traits under stimulus conditions: that is, the extent to which the environment affects the neurobiological functioning underlying the traits. To explore the nature of development of extreme values on these traits, each trait is discussed in terms of three major issues: (a) the neurobiological variables associated with the trait, (b) individual variation in this neurobiology as a function of genetic polymorphisms, and (c) the effects of environmental adversity on these neurobiological variables through the action of epigenetic processes. It is noted that gene–environment interaction appears to be dependent on two main factors: (a) both genetic and environmental variables appear to have the most profound and enduring effects when they exert their effects during early postnatal periods, times when the forebrain is undergoing exuberant experience–expectant dendritic and axonal growth; and (b) environmental effects on neurobiology are strongly modified by individual differences in “traitlike” functioning of neurobiological variables. A model of the nature of the interaction between environmental and neurobiological variables in the development of personality disturbance is presented.
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.
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.
Lifelines supports the theme that behavioral
development is a fluid, life-long phenomenon. In contrast, many
emotional and cognitive traits are subject to strong genetic
influence, and are highly stable over many years. The manner
in which neuroplasticity and trait stability cooccur needs to
be modeled. An outline of such a model is provided to promote
discussion of this complex issue.
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
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.
The commentaries on our target article address three
main areas: (1) the relative importance of extraversion and other
related traits to DA functioning, (2) how the long-term stability of
extraversion can be conceptualized within a highly plastic central
nervous system, and (3) the nature of DA functioning in the MOC
network and in extraversion. We have organized our Response,
therefore, into three major sections.
Email your librarian or administrator to recommend adding this to your organisation's collection.