Genetics of anxiety disorders

Arnold, Paul; Zai, Gwyneth; Richter, Margaret A.

doi:10.1007/s11920-004-0073-1

Cited by 61 publications

(25 citation statements)

References 116 publications

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“…Mirtazapine downregulated genes involved with cell cycle and brain development while paroxetine affected genes involved in metabolism and cell structure [87]. This technique could be used to investigate the roles of receptors such as, adenosine 2A, 5-HT 1A and 5-HT 2A which have been implicated in panic disorder [88] and 5-HT 1B , 5-HT 2A , dopamine D4, subunit 2B of ionotropic N-methyl-d-aspartate receptors implicated in obsessive-compulsive disorder [88].…”

Section: Molecular Genetic Approachesmentioning

confidence: 99%

Mechanisms of action of antidepressants: from neurotransmitter systems to signaling pathways

Taylor

Fricker

Devi

et al. 2005

Cellular Signalling

144

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Antidepressants are commonly used in the treatment of anxiety and depression, medical conditions that affect ~17-20% of the population. The clinical effects of antidepressants take several weeks to manifest, suggesting that these drugs induce adaptive changes in brain structures affected by anxiety and depression. In order to develop shorter-acting and more effective drugs for the treatment of anxiety and depression, it is important to understand how antidepressants bring about their beneficial effects. Recent reports suggest that antidepressants can induce neurogenesis in the adult brain, although the mechanisms involved are not clearly understood. In this review, we describe the different neurotransmitter systems that are affected by anxiety and depression and how they are modulated by antidepressant treatment with a focus on signaling molecules and pathways that are activated during neurotransmitter receptor induced neurogenesis.

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Section: Molecular Genetic Approachesmentioning

confidence: 99%

Mechanisms of action of antidepressants: from neurotransmitter systems to signaling pathways

Taylor

Fricker

Devi

et al. 2005

Cellular Signalling

144

View full text Add to dashboard Cite

show abstract

“…Low HA has been associated with risk-taking, harmful behavior, impulsiveness, suicidal ideation, and aggression (Cloninger, 1986;Peirson, Heuchert, Thomala, Berk, Plein, & Cloninger, 1999), whilst high HA has been associated with behavioral inhibition, anxiety and neuroticism (Carver & Miller, 2006). HA is referred to as the anxietyrelated personality dimension (Montag, Reuter, Jurkiewicz, Markett, & Panksepp, 2013), and therefore high HA levels are tightly associated with neurobiological pathologies such as depression and anxiety (Arnold, Zai, & Richter, 2004;Commons, Connolley, & Valentino, 2003;Kenna, RoderHanna, Leggio, Zywiak, Clifford, Edwards, & Swift, 2012;Westlye, Bjornebekk, Grydeland, Fjell, & Walhovd, 2011).…”

Section: Robertmentioning

confidence: 99%

Dorsal raphe nucleus and harm avoidance: A resting-state investigation

Meylakh

Henderson

2016

Cogn Affect Behav Neurosci

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The temperament dimension of harm avoidance defines an individual's biological tendency to exhibit altering levels of anxious, inhibiting, and cautious behavior. High harm avoidance and anxiety are highly comorbid, likely due to activity in similar neural circuitries involving the dorsal raphe nucleus. Despite the many investigations that have explored personality factors and brain function, none have determined the influence of ongoing activity within dorsal raphe networks on harm avoidance. The aim of this study was to explore such a relationship. In 62 healthy subjects, a series of 180 functional magnetic resonance images covering the entire brain were collected, and each subject completed the 240-item TCI-R questionnaire. Independent component analyses were performed to define the dorsal raphe network and then to determine the regions significantly correlated with harm avoidance. The independent component analyses revealed three signal intensity fluctuation maps encompassing the dorsal raphe nucleus, showing interactions with regions of the amygdala, hippocampus, nucleus accumbens, and prefrontal, insular, and cingulate cortices. Within these systems, the resting signal intensity was significantly coupled to harm avoidance in the bilateral basal amygdala, bilateral ventral hippocampus, bilateral insula, bilateral nucleus accumbens, and medial prefrontal cortex. Note that we could not measure serotonergic output, but instead measured signal changes in the dorsal raphe that likely reflect synaptic activity. These data provide evidence that at rest, signal intensity fluctuations within the dorsal raphe networks are related to harm avoidance. Given the strong relationship between harm avoidance and anxiety-like behaviors, it is possible that ongoing activity within this identified neural circuitry can contribute to an individual developing anxiety disorders.

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“…Neuroticism is associated with bloodstream hormone and neurotransmitter release. Lower functioning of the neurotransmitter serotonin is related to the vulnerability to negative emotion (Arnold, Zai, and Richter 2004). Neuroticism is also associated with higher levels of norepinephrine (adrenaline) (Hennig 2004;Zuckerman 2005) and a higher baseline level of the stress hormone cortisol (Netter 2004).…”

Section: The Biological Basis Of the Five-factor Modelmentioning

confidence: 99%