What is the meaning of associations between personality traits and anxiety and depressive disorders?

Bienvenu, O. Joseph

doi:10.1590/s1516-44462007000100002

Cited by 8 publications

(9 citation statements)

References 5 publications

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“…Bienvenu et al (2004) had also detected higher neuroticism in patients with current PD as compared to those in remission. Although high neuroticism was proposed to predict later onset of anxiety disorders (Bienvenu, 2007), none of SSP personality traits significantly differed between patients with earlier (<30 years) and late (>29 years) onset of PD in our sample. Previous studies have found that low extraversion and low trust were associated with both agoraphobia and social phobia, but not with depression (Bienvenu, Brown, et al, 2001;Bienvenu, Nestadt, et al, 2001;Bienvenu et al, 2004).…”

Section: Neuroticism Extraversion Aggressivenesscontrasting

confidence: 71%

Evaluation of personality traits in panic disorder using Swedish universities Scales of Personality

Võhma¹,

Aluoja²,

Vasar³

et al. 2010

Journal of Anxiety Disorders

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Section: Neuroticism Extraversion Aggressivenesscontrasting

confidence: 71%

Evaluation of personality traits in panic disorder using Swedish universities Scales of Personality

Võhma¹,

Aluoja²,

Vasar³

et al. 2010

Journal of Anxiety Disorders

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“…In conclusion, our data suggest that chronic exposure to increased concentrations of glucocorticoids, as observed in various affective disorders (Plotsky et al, 1998; Barden, 2004; Gillespie and Nemeroff, 2005; Graeff, 2007; Gunduz-Bruce et al, 2007), Cushing’s syndrome (Sonino et al, 1998; Michaud et al, 2009; Pereira et al, 2010), or after prolonged stress exposure (Leonard, 2005; Herman et al, 2008; McEuen et al, 2008; Kyrou and Tsigos, 2009), is sufficient to elevate tph2 expression, induce a depression-like syndrome, flatten the diurnal HPA axis rhythm, and alter both glucose metabolism and weight gain. Our results indicate that dysregulation of circulating glucocorticoid concentrations and rhythmicity, independent from exposure to external stressors, disrupt the diurnal pattern of serotonin synthesis, and thus contribute to the dysfunction of circadian rhythms symptomatic of many psychiatric disorders, specifically affective disorders.…”

Section: Resultsmentioning

confidence: 50%

“…Thus, although tph2 mRNA expression varies in a diurnal manner throughout the entire DR, diurnal variations in TPH protein seem most pronounced in neural systems regulating circadian function, such as the SCN. This has important implications for patients suffering from affective disorders as many of them suffer from dysfunctions of circadian rhythms, including HPA axis rhythmicity (Deuschle et al, 1997; Gillespie and Nemeroff, 2005; Graeff, 2007; Wichers et al, 2008a), sleep-wake cycles (Pandi-Perumal et al, 2009; Westrich and Sprouse, 2010), and body temperature (Rausch et al, 2003; Bunney and Potkin, 2008). …”

Section: Discussionmentioning

confidence: 99%

“…Dysregulation of hypothalamic-pituitary-adrenal (HPA) axis functionality (Daban et al, 2005; Graeff, 2007; Pariante and Lightman, 2008; Walker et al, 2008) and brain serotonergic systems (Mann et al, 1989; Owens and Nemeroff, 1994; Naughton et al, 2000; Arango et al, 2002; Zill et al, 2004; De Luca et al, 2005; You et al, 2005) is a common feature of many stress-related psychiatric disorders, including major depressive disorder (MDD), bipolar disorder, and anxiety disorders. Meanwhile, various animal models of depression have been validated, in part, because of their impairments in emotionality together with HPA axis- and serotonergic dysfunctions (Neumann et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

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Chronic non-invasive corticosterone administration abolishes the diurnal pattern of tph2 expression

Donner

Montoya

Lukkes

et al. 2012

Psychoneuroendocrinology

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Both hypothalamic-pituitary-adrenal (HPA) axis activity and serotonergic systems are commonly dysregulated in stress-related psychiatric disorders. We describe here a non-invasive rat model for hypercortisolism, as observed in major depression, and its effects on physiology, behavior, and the expression of tph2, the gene encoding tryptophan hydroxylase 2, the rate-limiting enzyme for brain serotonin (5-hydroxytryptamine; 5-HT) synthesis. We delivered corticosterone (40 µg/ml, 100 µg/ml or 400 µg/ml) or vehicle to adrenal-intact adult, male rats via the drinking water for three weeks. On days 15, 16, 17 and 18, respectively, the rats’ emotionality was assessed in the open-field (OF), social interaction (SI), elevated plus-maze (EPM), and forced swim tests (FST). On day 21, half of the rats in each group were killed 2 h into the dark phase of a 12/12 h reversed light/dark cycle; the other half were killed 2 h into the light phase. We then measured indices of HPA axis activity, plasma glucose and interleukin-6 (IL-6) availability, and neuronal tph2 expression at each time point. Chronic corticosterone intake was sufficient to cause increased anxiety- and depressive-like behavior in a dose-dependent manner. It also disrupted the diurnal pattern of plasma adrenocorticotropin (ACTH), corticosterone, and glucose concentrations, caused adrenal atrophy, and prevented regular weight gain. No diurnal or treatment-dependent changes were found for plasma levels of IL-6. Remarkably, all doses of corticosterone treatment abolished the diurnal variation of tph2 mRNA expression in the brainstem dorsal raphe nucleus (DR) by elevating the gene’s expression during the animals’ inactive (light) phase. Our data demonstrate that chronic elevation of corticosterone creates a vulnerability to a depression-like syndrome that is associated with increased tph2 expression, similar to that observed in depressed patients.

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“…Panic disorder patients suffer from sudden brief periods of intense fear, hypervigilance, and distress, including autonomic symptoms like tachycardia, difficulty breathing, or nausea, without significant hypothalamic–pituitary–adrenal (HPA) axis stress responses [135]. Panic attacks can be, but do not have to be, triggered by specific stimuli, and the prevalence for panic disorder is two to three times as high in women as in men [127, 199, 396].…”

Section: Human Gender Differences In Anxiety and Emotional Disordersmentioning

confidence: 99%

Sex differences in anxiety and emotional behavior

Donner

Lowry

2013

Pflugers Arch - Eur J Physiol

298

170

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Research has elucidated causal links between stress exposure and the development of anxiety disorders, but due to the limited use of female or sex-comparative animal models, little is known about the mechanisms underlying sex differences in those disorders. This is despite an overwhelming wealth of evidence from the clinical literature that the prevalence of anxiety disorders is about twice as high in women compared to men, in addition to gender differences in severity and treatment efficacy. We here review human gender differences in generalized anxiety disorder, panic disorder, posttraumatic stress disorder and anxiety-relevant biological functions, discuss the limitations of classic conflict anxiety tests to measure naturally occurring sex differences in anxiety-like behaviors, describe sex-dependent manifestation of anxiety states after gestational, neonatal, or adolescent stressors, and present animal models of chronic anxiety states induced by acute or chronic stressors during adulthood. Potential mechanisms underlying sex differences in stress-related anxiety states include emerging evidence supporting the existence of two anatomically and functionally distinct serotonergic circuits that are related to the modulation of conflict anxiety and panic-like anxiety, respectively. We discuss how these serotonergic circuits may be controlled by reproductive steroid hormone-dependent modulation of crfr1 and crfr2 expression in the midbrain dorsal raphe nucleus and by estrous stage-dependent alterations of γ-aminobutyric acid (GABAergic) neurotransmission in the periaqueductal gray, ultimately leading to sex differences in emotional behavior.

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What is the meaning of associations between personality traits and anxiety and depressive disorders?

Cited by 8 publications

References 5 publications

Evaluation of personality traits in panic disorder using Swedish universities Scales of Personality

Evaluation of personality traits in panic disorder using Swedish universities Scales of Personality

Chronic non-invasive corticosterone administration abolishes the diurnal pattern of tph2 expression

Sex differences in anxiety and emotional behavior

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