Summary

Putting together a biosocial-levels approach to personality is like assembling the pieces of a jigsaw puzzle or fitting words into a crossword puzzle. In the jigsaw puzzle, one has two pieces that seem to be related but require a third piece to fit them together. In the crossword puzzle, horizontal words (relationships between traits and behaviors) require vertical words (between traits and behaviors and underlying biological traits) to confirm them. The puzzle for sensation seeking is beginning to form some semblance of a theoretical model, although many pieces are missing and many words are disconnected. The comparative approach relies on connecting findings from human correlational studies, using normal and disordered populations, with animal experimental and correlational data.

At the bottom of the puzzle, we find alleles of specific genes related to the trait at the top level and to its behavioral expressions. Alleles of a dopamine receptor gene (DRD4) and a serotonin transporter gene (5-HTTLPR) in interaction seem to be involved in (1) the trait of sensation seeking in adults; (2) behavioral expressions such as orientation, activity, and emotional reactivity in infants; (3) positive reactions to novelty in children; and (4) psycho-pathologies such as opiate use, attention-deficit/hyperactivity disorder, and pathological gambling. These genetic variations account for only a small part of the genetic variance, however, and other genes (pieces of the puzzle) remain to be discovered.

At the next levels, we find serotonin and dopamine neurotransmitter activity related to the sensation-seeking trait, probably also in interaction. Studies on other species and some human correlational research suggest that these neurotransmitters and their receptors in particular areas of the brain are involved in the personality trait. Dopamine reactivity is involved in approach behavior to novel stimuli and environments, whereas serotonergic reactivity is implicated in inhibition or passive avoidance of risky behavior in novel situations. Enzymes like MAO, which regulate the neurotransmitters, show similar relationships with traits and behaviors. Gonadal hormones and hormones in the HYPAC stress response system are also involved, although their effects on the neurotransmitters are not clear. Norepinephrine and cortisol seem to be involved in producing inhibition at the opposite pole of the disinhibition dimension.

At the level of psychophysiology, we find that sensation seekers have strong orienting responses to novel stimuli, which habituate quickly on repetititon. Dopamine has not yet been connected with this behavior, although it is interesting that the dopamine-serotonergic gene interaction affects orientation in young infants (Ebstein & Auerbach, 2002). The first definition of sensation seeking included the need for novel stimuli and experiences. The current definition (Zuckerman, 1994) adds intensity to the qualities of stimuli that are attractive to high sensation seekers.

Intensity of stimuli is the major influence in the EP augmenting-reducing (A-R) paradigm. In three species (human, cat, rat), augmenting of the cortical EP in response to increasing stimulus intensity is related to disinhibited impulsive behavior. Connections between the A-R paradigm and dopamine and serotonin also fit neatly into the model. Cortical augmenting in response to intense stimuli may represent "strength of the nervous system," to use the old Pavlovian term.

The capacity to function and feel well in response to intense stimuli has an obvious adaptive value and plays a role in the risk taking related to sensation seeking. It may be a function of strong dopaminergic and weak serotonergic reactivity. Reducing seems to serve a protective function in the nervous system of low sensation seekers. It may be mediated by strong serotonergic or gamma-aminobutyric acid (GABA) activity triggered by intense stimuli.

The theoretical model proposed here is pictured in Figure 3.3. Essentially, Impulsive Unsocialized Sensation Seeking (P-ImpUSS) is a function of the relative strengths and interactions of three behavioral mechanisms: approach, inhibition, and arousal. The biochemical mechanisms underlying these are also shown in the figure. Note that interactions occur at all of the biological levels. Simple isomorphisms, like those shown between the behavioral mechanisms and the neurotransmitters are unlikely. An accurate biosocial model would require arrows connecting everything with nearly everything else. It would also need more two-way arrows reflecting the interactions of behavior and biology in both directions, like the one between approach and inhibition. Although simple elegant models may be fine for physics, they are problematic for biobehavioral science, even at the most molecular levels such as the gene. We must simplify in order to converse in a coherent manner, recognizing that the subtext is more complex.

FIGURE 3.3. A psychopharmacological model for extraversion-sociability (E-Socia-bility), impulsive unsocialized sensation seeking (P-ImpUSS), and neuroticism-anxiety (N-Anxiety), showing the underlying behavioral mechanisms (approach, inhibition, and arousal) and neurotransmitters, enzymes, and hormones involved. Agonistic interactions between factors are indicated by a plus sign, and antagonistic interactions between factors are indicated by a minus sign. MAO, monoamine oxidase; DBH, dopamine-beta-hydroxylase; GABA, gamma-aminobutyric acid. From Zuckerman (1995, Fig. 1, p. 331). Copyright 1995 by Blackwell Publishing, Ltd. Reprinted by per-

FIGURE 3.3. A psychopharmacological model for extraversion-sociability (E-Socia-bility), impulsive unsocialized sensation seeking (P-ImpUSS), and neuroticism-anxiety (N-Anxiety), showing the underlying behavioral mechanisms (approach, inhibition, and arousal) and neurotransmitters, enzymes, and hormones involved. Agonistic interactions between factors are indicated by a plus sign, and antagonistic interactions between factors are indicated by a minus sign. MAO, monoamine oxidase; DBH, dopamine-beta-hydroxylase; GABA, gamma-aminobutyric acid. From Zuckerman (1995, Fig. 1, p. 331). Copyright 1995 by Blackwell Publishing, Ltd. Reprinted by per-

Anxiety and Depression 101

Anxiety and Depression 101

Everything you ever wanted to know about. We have been discussing depression and anxiety and how different information that is out on the market only seems to target one particular cure for these two common conditions that seem to walk hand in hand.

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