Biology of mood & anxiety disorders最新文献

{"title":"Effects of genetic deletion of the Kv4.2 voltage-gated potassium channel on murine anxiety-, fear- and stress-related behaviors.","authors":"Carly Kiselycznyk,&nbsp;Dax A Hoffman,&nbsp;Andrew Holmes","doi":"10.1186/2045-5380-2-5","DOIUrl":"https://doi.org/10.1186/2045-5380-2-5","url":null,"abstract":"<p><strong>Background: </strong>Potassium channels have been proposed to play a role in mechanisms of neural plasticity, and the Kv4.2 subunit has been implicated in the regulation of action-potential back-propagation to the dendrites. Alterations in mechanisms of plasticity have been further proposed to underlie various psychiatric disorders, but the role of Kv4.2 in anxiety or depression is not well understood.</p><p><strong>Methods: </strong>In this paper, we analyzed the phenotype Kv4.2 knockout mice based on their neurological function, on a battery of behaviors including those related to anxiety and depression, and on plasticity-related learning tasks.</p><p><strong>Results: </strong>We found a novelty-induced hyperactive phenotype in knockout mice, and these mice also displayed increased reactivity to novel stimulus such as an auditory tone. No clear anxiety- or depression-related phenotype was observed, nor any alterations in learning/plasticity-based paradigms.</p><p><strong>Conclusions: </strong>We did not find clear evidence for an involvement of Kv4.2 in neuropsychiatric or plasticity-related phenotypes, but there was support for a role in Kv4.2 in dampening excitatory responses to novel stimuli.</p>","PeriodicalId":89532,"journal":{"name":"Biology of mood & anxiety disorders","volume":"2 ","pages":"5"},"PeriodicalIF":0.0,"publicationDate":"2012-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2045-5380-2-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30723481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Current understanding of the bi-directional relationship of major depression with inflammation.","authors":"Berhane Messay,&nbsp;Alvin Lim,&nbsp;Anna L Marsland","doi":"10.1186/2045-5380-2-4","DOIUrl":"https://doi.org/10.1186/2045-5380-2-4","url":null,"abstract":"<p><p> Consistent evidence links major depression and its affective components to negative health outcomes. Although the pathways of these effects are likely complex and multifactorial, recent evidence suggests that innate inflammatory processes may play a role. An overview of current literature suggests that pathways between negative moods and inflammation are bi-directional. Indeed, negative moods activate peripheral physiologic mechanisms that result in an up regulation of systemic levels of inflammation. Conversely, peripheral inflammatory mediators signal the brain to affect behavioral, affective and cognitive changes that are consistent with symptoms of major depressive disorder. It is likely that these pathways are part of a complex feedback loop that involves the nervous, endocrine, and immune systems and plays a role in the modulation of peripheral inflammatory responses to central and peripheral stimuli, in central responses to peripheral immune activation and in the maintenance of homeostatic balance. Further research is warranted to fully understand the role of central processes in this feedback loop, which likely contributes to the pathophysiology of mental and physical health.</p>","PeriodicalId":89532,"journal":{"name":"Biology of mood & anxiety disorders","volume":"2 ","pages":"4"},"PeriodicalIF":0.0,"publicationDate":"2012-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2045-5380-2-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30720983","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex differences, gonadal hormones and the fear extinction network: implications for anxiety disorders.","authors":"Kelimer Lebron-Milad,&nbsp;Mohammed R Milad","doi":"10.1186/2045-5380-2-3","DOIUrl":"https://doi.org/10.1186/2045-5380-2-3","url":null,"abstract":"<p><p> Convergent data from rodents and human studies have led to the development of models describing the neural mechanisms of fear extinction. Key components of the now well-characterized fear extinction network include the amygdala, hippocampus, and medial prefrontal cortical regions. These models are fueling novel hypotheses that are currently being tested with much refined experimental tools to examine the interactions within this network. Lagging far behind, however, is the examination of sex differences in this network and how sex hormones influence the functional activity and reactivity of these brain regions in the context of fear inhibition. Indeed, there is a large body of literature suggesting that sex hormones, such as estrogen, do modulate neural plasticity within the fear extinction network, especially in the hippocampus.After a brief overview of the fear extinction network, we summarize what is currently known about sex differences in fear extinction and the influence of gonadal hormones on the fear extinction network. We then go on to propose possible mechanisms by which sex hormones, such as estrogen, may influence neural plasticity within the fear extinction network. We end with a discussion of how knowledge to be gained from developing this line of research may have significant ramifications towards the etiology, epidemiology and treatment of anxiety disorders.</p>","PeriodicalId":89532,"journal":{"name":"Biology of mood & anxiety disorders","volume":"2 ","pages":"3"},"PeriodicalIF":0.0,"publicationDate":"2012-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2045-5380-2-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30722685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rumination in bipolar disorder: evidence for an unquiet mind.","authors":"Sharmin Ghaznavi,&nbsp;Thilo Deckersbach","doi":"10.1186/2045-5380-2-2","DOIUrl":"https://doi.org/10.1186/2045-5380-2-2","url":null,"abstract":"<p><p> Depression in bipolar disorder has long been thought to be a state characterized by mental inactivity. However, recent research demonstrates that patients with bipolar disorder engage in rumination, a form of self-focused repetitive cognitive activity, in depressed as well as in manic states. While rumination has long been associated with depressed states in major depressive disorder, the finding that patients with bipolar disorder ruminate in manic states is unique to bipolar disorder and challenges explanations put forward for why people ruminate. We review the research on rumination in bipolar disorder and propose that rumination in bipolar disorder, in both manic and depressed states, reflects executive dysfunction. We also review the neurobiology of bipolar disorder and recent neuroimaging studies of rumination, which is consistent with our hypothesis that the tendency to ruminate reflects executive dysfunction in bipolar disorder. Finally, we relate the neurobiology of rumination to the neurobiology of emotion regulation, which is disrupted in bipolar disorder.</p>","PeriodicalId":89532,"journal":{"name":"Biology of mood & anxiety disorders","volume":"2 ","pages":"2"},"PeriodicalIF":0.0,"publicationDate":"2012-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2045-5380-2-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30721840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional anomalies in healthy individuals with a first degree family history of major depressive disorder.","authors":"Francesco Amico,&nbsp;Angela Carballedo,&nbsp;Danuta Lisiecka,&nbsp;Andrew J Fagan,&nbsp;Gerard Boyle,&nbsp;Thomas Frodl","doi":"10.1186/2045-5380-2-1","DOIUrl":"https://doi.org/10.1186/2045-5380-2-1","url":null,"abstract":"<p><strong>Background: </strong>Individuals with major depressive disorder (MDD) process information with a bias towards negative stimuli. However, little is known on the link between vulnerability to MDD and brain functional anomalies associated with stimulus bias.</p><p><strong>Methods: </strong>A cohort of 38 subjects, of which 14 were patients with acute MDD and 24 were healthy controls (HC), were recruited and compared. The HC group included 10 healthy participants with a first degree family history of depression (FHP) and 14 volunteers with no family history of any psychiatric disease (FHN). Blood oxygen level dependence signals were acquired from functional magnetic resonance imaging (fMRI) during performance in a dot-probe task using fearful and neutral stimuli. Reaction times and the number of errors were also obtained.</p><p><strong>Results: </strong>Although MDD patients and HC showed no behavioral difference, the MDD group exhibited smaller activation in the left middle cingulum. The MDD group also showed smaller activation in the left insula when compared to the HC group or the FHN group. Finally, FHP participants exhibited higher activation in the right Heschl's gyrus compared to FHN participants.</p><p><strong>Conclusions: </strong>The present study shows that family risk for MDD is associated with increased activation in the Heschl's gyrus. Our results also suggest that acute MDD is linked to reduced activation in the insula and anterior cingulate cortex during processing of subliminal, not recognizable, masked fearful stimuli. Further research should confirm these results in a larger cohort of participants.</p>","PeriodicalId":89532,"journal":{"name":"Biology of mood & anxiety disorders","volume":"2 ","pages":"1"},"PeriodicalIF":0.0,"publicationDate":"2012-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2045-5380-2-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30720866","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Amygdala activation to threat under attentional load in individuals with anxiety disorder.","authors":"Thomas Straube,&nbsp;Judith Lipka,&nbsp;Andreas Sauer,&nbsp;Martin Mothes-Lasch,&nbsp;Wolfgang Hr Miltner","doi":"10.1186/2045-5380-1-12","DOIUrl":"https://doi.org/10.1186/2045-5380-1-12","url":null,"abstract":"<p><strong>Background: </strong>Previous studies in healthy subjects have shown that strong attentional distraction prevents the amygdala from responding to threat stimuli. Here, we investigated the effects of attentional load on amygdala activation to threat-related stimuli in individuals suffering from an anxiety disorder.</p><p><strong>Methods: </strong>During functional magnetic resonance imaging, spider-phobicand healthy control subjects were presented with phobia-related and neutral stimuli while performing a distraction task with varying perceptual load (high vs low).</p><p><strong>Results: </strong>Our data revealed a pattern of simultaneously increased amygdala and visual cortical activation to threat vs neutral pictures in phobic individuals, compared with controls, occurring regardless of attentional load.</p><p><strong>Conclusions: </strong>These results suggest that, in contrast to studies in healthy subjects, amygdala activation to clinically relevant threat stimuli is more resistant to attentional load.</p>","PeriodicalId":89532,"journal":{"name":"Biology of mood & anxiety disorders","volume":"1 1","pages":"12"},"PeriodicalIF":0.0,"publicationDate":"2011-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2045-5380-1-12","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30720491","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Frontostriatal functional connectivity in major depressive disorder.","authors":"Daniella J Furman,&nbsp;J Paul Hamilton,&nbsp;Ian H Gotlib","doi":"10.1186/2045-5380-1-11","DOIUrl":"https://doi.org/10.1186/2045-5380-1-11","url":null,"abstract":"<p><strong>Background: </strong>Abnormalities of the striatum and frontal cortex have been reported consistently in studies of neural structure and function in major depressive disorder (MDD). Despite speculation that compromised connectivity between these regions may underlie symptoms of MDD, little work has investigated the integrity of frontostriatal circuits in this disorder.</p><p><strong>Methods: </strong>Functional magnetic resonance images were acquired from 21 currently depressed and 19 never-disordered women during wakeful rest. Using four predefined striatal regions-of-interest, seed-to-whole brain correlations were computed and compared between groups.</p><p><strong>Results: </strong>Compared to controls, depressed participants exhibited attenuated functional connectivity between the ventral striatum and both ventromedial prefrontal cortex and subgenual anterior cingulate cortex. Depressed participants also exhibited stronger connectivity between the dorsal caudate and dorsal prefrontal cortex, which was positively correlated with severity of the disorder.</p><p><strong>Conclusions: </strong>Depressed individuals are characterized by aberrant connectivity in frontostriatal circuits that are posited to support affective and cognitive processing. Further research is required to examine more explicitly the link between patterns of disrupted connectivity and specific symptoms of depression, and the extent to which these patterns precede the onset of depression and normalize with recovery from depressive illness.</p>","PeriodicalId":89532,"journal":{"name":"Biology of mood & anxiety disorders","volume":"1 1","pages":"11"},"PeriodicalIF":0.0,"publicationDate":"2011-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2045-5380-1-11","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30721776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Criteria of validity for animal models of psychiatric disorders: focus on anxiety disorders and depression.","authors":"Catherine Belzung,&nbsp;Maël Lemoine","doi":"10.1186/2045-5380-1-9","DOIUrl":"https://doi.org/10.1186/2045-5380-1-9","url":null,"abstract":"<p><p> Animal models of psychiatric disorders are usually discussed with regard to three criteria first elaborated by Willner; face, predictive and construct validity. Here, we draw the history of these concepts and then try to redraw and refine these criteria, using the framework of the diathesis model of depression that has been proposed by several authors. We thus propose a set of five major criteria (with sub-categories for some of them); homological validity (including species validity and strain validity), pathogenic validity (including ontopathogenic validity and triggering validity), mechanistic validity, face validity (including ethological and biomarker validity) and predictive validity (including induction and remission validity). Homological validity requires that an adequate species and strain be chosen: considering species validity, primates will be considered to have a higher score than drosophila, and considering strains, a high stress reactivity in a strain scores higher than a low stress reactivity in another strain. Pathological validity corresponds to the fact that, in order to shape pathological characteristics, the organism has been manipulated both during the developmental period (for example, maternal separation: ontopathogenic validity) and during adulthood (for example, stress: triggering validity). Mechanistic validity corresponds to the fact that the cognitive (for example, cognitive bias) or biological mechanisms (such as dysfunction of the hormonal stress axis regulation) underlying the disorder are identical in both humans and animals. Face validity corresponds to the observable behavioral (ethological validity) or biological (biomarker validity) outcomes: for example anhedonic behavior (ethological validity) or elevated corticosterone (biomarker validity). Finally, predictive validity corresponds to the identity of the relationship between the triggering factor and the outcome (induction validity) and between the effects of the treatments on the two organisms (remission validity). The relevance of this framework is then discussed regarding various animal models of depression.</p>","PeriodicalId":89532,"journal":{"name":"Biology of mood & anxiety disorders","volume":"1 1","pages":"9"},"PeriodicalIF":0.0,"publicationDate":"2011-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2045-5380-1-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30722142","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Facial emotion processing in major depression: a systematic review of neuroimaging findings.","authors":"Anja Stuhrmann,&nbsp;Thomas Suslow,&nbsp;Udo Dannlowski","doi":"10.1186/2045-5380-1-10","DOIUrl":"https://doi.org/10.1186/2045-5380-1-10","url":null,"abstract":"<p><strong>Background: </strong>Cognitive models of depression suggest that major depression is characterized by biased facial emotion processing, making facial stimuli particularly valuable for neuroimaging research on the neurobiological correlates of depression. The present review provides an overview of functional neuroimaging studies on abnormal facial emotion processing in major depression. Our main objective was to describe neurobiological differences between depressed patients with major depressive disorder (MDD) and healthy controls (HCs) regarding brain responsiveness to facial expressions and, furthermore, to delineate altered neural activation patterns associated with mood-congruent processing bias and to integrate these data with recent functional connectivity results. We further discuss methodological aspects potentially explaining the heterogeneity of results.</p><p><strong>Methods: </strong>A Medline search was performed up to August 2011 in order to identify studies on emotional face processing in acutely depressed patients compared with HCs. A total of 25 studies using functional magnetic resonance imaging were reviewed.</p><p><strong>Results: </strong>The analysis of neural activation data showed abnormalities in MDD patients in a common face processing network, pointing to mood-congruent processing bias (hyperactivation to negative and hypoactivation to positive stimuli) particularly in the amygdala, insula, parahippocampal gyrus, fusiform face area, and putamen. Furthermore, abnormal activation patterns were repeatedly found in parts of the cingulate gyrus and the orbitofrontal cortex, which are extended by investigations implementing functional connectivity analysis. However, despite several converging findings, some inconsistencies are observed, particularly in prefrontal areas, probably caused by heterogeneities in paradigms and patient samples.</p><p><strong>Conclusions: </strong>Further studies in remitted patients and high-risk samples are required to discern whether the described abnormalities represent state or trait characteristics of depression.</p>","PeriodicalId":89532,"journal":{"name":"Biology of mood & anxiety disorders","volume":"1 1","pages":"10"},"PeriodicalIF":0.0,"publicationDate":"2011-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2045-5380-1-10","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30724006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An fMRI study of unconditioned responses in post-traumatic stress disorder.","authors":"Clas Linnman,&nbsp;Thomas A Zeffiro,&nbsp;Roger K Pitman,&nbsp;Mohammed R Milad","doi":"10.1186/2045-5380-1-8","DOIUrl":"https://doi.org/10.1186/2045-5380-1-8","url":null,"abstract":"<p><strong>Background: </strong>Both fear and pain processing are altered in post-traumatic stress disorder (PTSD), as evidenced by functional neuroimaging studies showing increased amygdala responses to threats, and increased insula, putamen and caudate activity in response to heat pain. Using psychophysiology and functional magnetic resonance imaging, we studied conditioned and unconditioned autonomic and neuronal responses in subjects with PTSD versus trauma-exposed non-PTSD control (TENC) subjects. A design using an electric shock selected by subjects to be 'highly annoying but not painful' as an unconditioned stimulus (US) with partially reinforced cues allowed us to partly disentangle the expectancy- and prediction-error components from sensory components of the unconditioned response.</p><p><strong>Results: </strong>Whereas responses to the conditioned stimulus (CS) were similar in PTSD and TENC, the former displayed higher putamen, insula, caudate and amygdala responses to the US. Reactivity to the US in the anterior insula correlated with PTSD symptom severity. Functional connectivity analyses using the putamen as a seed region indicated that TENC subjects had increased amygdala-putamen connectivity during US delivery; this connection was disengaged in PTSD.</p><p><strong>Conclusions: </strong>Our results indicate that although neural processing of fear learning in people with PTSD seems to be comparable with controls, neural responses to unconditioned aversive stimuli in PTSD seem to be increased.</p>","PeriodicalId":89532,"journal":{"name":"Biology of mood & anxiety disorders","volume":"1 1","pages":"8"},"PeriodicalIF":0.0,"publicationDate":"2011-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/2045-5380-1-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"30721829","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}