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PubMed2006

Examining the state-trait anxiety relationship: a behavioural genetic approach.

State and trait anxiety define different aspects of anxiety, and may represent environmentally and genetically mediated components of this phenotype. Furthermore their relationship, where trait anxiety is expressed through levels of state anxiety under threatening circumstances, may represent a process of interplay between a genetic vulnerability factor and an environmental stressor. To test these hypotheses, we explored genetic and environmental influences on measures of state and trait anxiety in a sample of 1058 twins (521 males and 537 females) aged 8-16. The results were consistent with these hypotheses. State anxiety is largely influenced by environmental factors in males and females whereas trait anxiety shows moderate genetic effects and substantial non-shared environment effects. Their association was accounted for by non-shared environmental effects, with modest genetic and shared environmental inputs. The implications of these results for vulnerability mechanisms involving stress reactivity on anxiety are discussed.

Adolescent↗
PubMed1989

The measurement of suicidality, aggressivity and impulsivity.

1. From an evolutionary point of view aggressive behavior increases the chances of individual survival as well as inclusive fitness. 2. There are brain structures and biochemical systems that are involved in the regulation of aggressive behavior. 3. Genetic studies have revealed genetic contributions to aggressive as well as impulsive behaviors. 4. Research has demonstrated correlations between measures of suicidality, violence and impulsivity. 5. A two-step model of countervailing forces has been developed that identifies amplifiers and attenuators of the aggressive impulse. This model has enabled us to determine a set of variables that influence suicide but not violence and another set that influences violence but not suicide.

Aggression↗
PubMed1991

Influence of psychogenetics in opiate tolerance and abstinence in mice.

1. Four different strains of mice were used to study the influence of psychogenetics in opiate tolerance and abstinence. 2. The CD1 strain seemed to be more sensitive to naloxone administration after four days of morphine implantation, because administration of the antagonist induces a number of jumps in the withdrawal phase higher than in the case of the DBA or C3H strains. 3. DBA and C3H mice elicit analgesia before the CD1 strain, whereas the C3H mice lose body weight at a faster rate than the other strains. 4. C57 bl mice died after morphine implantation (100%). 5. These findings are discussed in relation with neurochemical and receptor variations.

Animals↗
PubMed2003

Opposite metabolic changes in the habenula and ventral tegmental area of a genetic model of helpless behavior.

Congenitally helpless rats have been selectively bred to display an immediate helpless response to stress in order to model hereditary brain differences that contribute to depression vulnerability. Differences in regional brain metabolism between congenitally helpless and non-helpless rats were investigated using quantitative cytochrome oxidase histochemistry. The results indicated that congenitally helpless rats had 64-71% elevated metabolism in the habenula and a 25% elevation in the related interpeduncular nucleus. In contrast, helpless rats had 28% reduced metabolism in the ventral tegmental area (VTA) and 14-16% reductions in the basal ganglia and basolateral and central amygdala. The opposite metabolic changes in the habenula and ventral tegmental area may be especially important for determining the congenitally helpless rat's global pattern of brain activity, which resembles the metabolic activity pattern produced by dopamine antagonism.

Animals↗
PubMed2006

The cognitive genetics of attention deficit hyperactivity disorder (ADHD): sustained attention as a candidate phenotype.

Here we describe the application of cognitive genetics to the study of attention deficit hyperactivity disorder (ADHD). Cognitive genetics owes much to the pioneering work of cognitive neuropsychologists such as John Marshall, whose careful observations of cognitive dissociations between brain-lesioned patients greatly advanced the theoretical understanding of normal cognitive function. These theories have in turn helped to constrain linkages between candidate genes and cognitive processes and thus help to drive the relatively new field of cognitive genetics in a hypothesis-driven fashion. We examined the relationship between sustained attention deficits in ADHD and genetic variation in a catecholamine-related gene, dopamine beta hydroxylase (DbetaH). DBH encodes the enzyme that converts dopamine to noradrenaline and is crucial to catecholamine regulation. A polymorphism with the DBH gene has been associated with ADHD. In fifty-two children with ADHD, we examined whether variation in the Taq I DBH gene polymorphism was related to sustained attention performance. Participants performed the Sustained Attention to Response Test (SART). Performance on the SART discriminates ADHD from control children, and in imaging work, is associated with right frontoparietal activation. A significant effect of DBH genotype was found on SART performance measures. Children possessing two copies of the ADHD-associated risk allele (A2) had significantly poorer sustained attention than those ADHD children who did not possess this allele or a non-genotyped control group. The DBH gene may contribute to the susceptibility for ADHD, in part because of its varying effects on the development of brain mechanisms mediating sustained attention.

Adolescent↗