Reduced Serotonin Type 1<sub>A</sub>Receptor Binding in Panic Disorder: Figure 1.

Neumeister, Alexander; Bain, Earle; Nugent, Allison C.; Carson, Richard E.; Bonne, Omer; Luckenbaugh, David A.; Eckelman, William C.; Herscovitch, Peter; Charney, Dennis S.; Drevets, Wayne C.

doi:10.1523/jneurosci.4921-03.2004

Cited by 345 publications

(259 citation statements)

References 13 publications

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“…This may ultimately cause reduced 5-HT neurotransmission, perhaps predisposing individuals to depression and suicidal behavior. 58 Keeping in mind that the abnormalities in 5-HT 1A receptor binding are not specific for depression, 60 this finding may reflect a general vulnerability factor for psychopathology, including affective and anxiety-related disorders.…”

Section: -Ht Transportermentioning

confidence: 86%

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

et al. 2006

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In recent years, the term serotonergic vulnerability (SV) has been used in scientific literature, but so far it has not been explicitly defined. This review article attempts to elucidate the SV concept. SV can be defined as increased sensitivity to natural or experimental alterations of the serotonergic (5-HTergic) system. Several factors that may disrupt the 5-HTergic system and hence contribute to SV are discussed, including genetic factors, female gender, personality characteristics, several types of stress and drug use. It is explained that SV can be demonstrated by means of manipulations of the 5-HTergic system, such as 5-HT challenges or acute tryptophan depletion (ATD). Results of 5-HT challenge studies and ATD studies are discussed in terms of their implications for the concept of SV. A model is proposed in which a combination of various factors that may compromise 5-HT functioning in one person can result in depression or other 5-HT-related pathology. By manipulating 5-HT levels, in particular with ATD, vulnerable subjects may be identified before pathology initiates, providing the opportunity to take preventive action. Although it is not likely that this model applies to all cases of depression, or is able to identify all vulnerable subjects, the strength of the model is that it may enable identification of vulnerable subjects before the 5-HT related pathology occurs. Molecular Psychiatry ( Keywords: serotonin; mood disorders; stress; genetics; sex; tryptophan Involvement of serotonin in depressionMood disorders are one of the most prevalent forms of mental illness. 1 According to the DSM-IV, the lifetime risk for major depressive disorder is between 10 and 25% for women and between 5 and 12% for men. 2 Depression has been studied intensively during the last few decades, but the psychological and neurobiological determinants of depression have not yet been precisely defined. Although several factors are known to contribute to the etiology of depression, it is not clear how these factors cause depression, and why some subjects become depressed while others remain unaffected. In terms of biological factors in the etiology of depression, there are several hypotheses. These include neurotransmitter dysfunctions (serotonin, 5-HT; dopamine, DA; norepinephrine, NE); dysregulations in hypothalamic-pituitary-adrenal (HPA) axis activity; and immune system imbalance. The aim of this article is not to discuss all of these hypotheses in detail, but to evaluate the role that serotonin may play within these hypothesized mechanisms.It is widely accepted that diminished serotonergic (5-HTergic) function is involved in the onset and course of depression. 3,4 The 5-HTergic system is a large and complex system. Although nearly all cell bodies of 5-HTergic neurons are located in the raphe nuclei in the brain stem, the axons of these neurons innervate almost the entire brain. The actions of 5-HT are mediated by 16 types and subtypes of receptors. 5 As the 5-HTergic system is assumed to be a modulatory system, the exact func...

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Section: -Ht Transportermentioning

confidence: 86%

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

et al. 2006

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“…Previous studies used only self-report of current depressive symptom ratings, which may not be optimal because the lack of effect of selective serotonin reuptake inhibitor treatment and hydrocortisone challenge on 5-HT 1A receptors in recovered patients with MDD suggests state-independence of reduced 5-HT 1A receptor BP in depression (4,5). Moreover, increased prevalence of anxiety disorders in epilepsy (24) and reduced 5-HT 1A receptor BP in panic disorder (39) appear to make an evaluation of the role of comorbid anxiety disorders, as included in the current study, necessary, although it has to be kept in mind that anxiety and depression may be alternative manifestations of the same underlying diathesis rather than independent disorders (34). Sample size and appropriate psychiatric assessment may have contributed to the relatively clear results and made a detailed evaluation of possible effect modifiers including laterality, focus side, MTS, gender, current major depressive episode and comorbid anxiety disorders possible.…”

Section: Discussionmentioning

confidence: 99%

5-HT1A Receptor Binding in Temporal Lobe Epilepsy Patients With and Without Major Depression

Hasler

Bonwetsch

Giovacchini

et al. 2007

Biological Psychiatry

129

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Background-Major depressive disorder (MDD) is the most common comorbid psychiatric condition associated with temporal lobe epilepsy (TLE). Preclinical and clinical studies suggest that 5-HT 1A receptors play a role in the pathophysiology of both TLE and MDD. There is preliminary evidence for an association between decreased 5-HT 1A receptor binding in limbic brain areas and affective symptoms in TLE patients. The objective of this study was to compare 5-HT 1A receptor binding between TLE patients with and without MDD. For the first time, 5-HT 1A receptor binding was measured in a sample large enough to permit sensitive comparisons between TLE patients with and without comorbid MDD diagnosed by clinical and structured psychiatric interviews.

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“…Parsey (145) found no difference in carbonyl- 11 C]WAY100635 BP in MDD, although a subgroup of never medicated subjects had elevated carbonyl-11 C]WAY100635 BP. Recent studies have found reduced [ 11 C] WAY100635 BP in social phobia (146) and panic disorder (147). These findings suggest ED, mood, and depression share disturbances of common systems but are etiologically different.…”

Section: -Ht 1a Receptormentioning

confidence: 98%

Neurobiology of anorexia and bulimia nervosa

Kaye

2008

Physiology & Behavior

527

369

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Reduced Serotonin Type 1_AReceptor Binding in Panic Disorder: Figure 1.

Cited by 345 publications

References 13 publications

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

5-HT1A Receptor Binding in Temporal Lobe Epilepsy Patients With and Without Major Depression

Neurobiology of anorexia and bulimia nervosa

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Reduced Serotonin Type 1AReceptor Binding in Panic Disorder: Figure 1.

Cited by 345 publications

References 13 publications

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

Serotonergic vulnerability and depression: assumptions, experimental evidence and implications

5-HT1A Receptor Binding in Temporal Lobe Epilepsy Patients With and Without Major Depression

Neurobiology of anorexia and bulimia nervosa

Contact Info

Product

Resources

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Reduced Serotonin Type 1_AReceptor Binding in Panic Disorder: Figure 1.