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Adolescence is a neuroplastic period for self-processing and emotion regulation transformations, that if derailed, are linked to persistent depression. Neural mechanisms of adolescent self-processing and emotion regulation ought to be targeted via new treatments, given moderate effectiveness of current interventions. Thus, we implemented a novel neurofeedback protocol in adolescents to test the engagement of circuits sub-serving self-processing and emotion regulation.MethodsDepressed (n = 34) and healthy (n = 19) adolescents underwent neurofeedback training using a novel task. They saw their happy face as a cue to recall positive memories and increased displayed amygdala and hippocampus activity. The control condition was counting-backwards while viewing another happy face. A self vs. other face recognition task was administered before and after neurofeedback training.ResultsAdolescents showed higher frontotemporal activity during neurofeedback and higher amygdala and hippocampus and hippocampi activity in time series and region of interest analyses respectively. Before neurofeedback there was higher saliency network engagement for self-face recognition, but that network engagement was lower after neurofeedback. Depressed youth exhibited higher fusiform, inferior parietal lobule and cuneus activity during neurofeedback, but controls appeared to increase amygdala and hippocampus activity faster compared to depressed adolescents.ConclusionsNeurofeedback recruited frontotemporal cortices that support social cognition and emotion regulation. Amygdala and hippocampus engagement via neurofeedback appears to change limbic-frontotemporal networks during self-face recognition. A placebo group or condition and contrasting amygdala and hippocampus, hippocampi or right amygdala versus frontal loci of neurofeedback, e.g. dorsal anterior cingulate cortex, with longer duration of neurofeedback training will elucidate dosage and loci of neurofeedback in adolescents.  相似文献   
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BackgroundImpulsive aggressive behavior is thought to be facilitated by activation of the limbic brain, particularly the amygdala and hippocampus., Functional imaging studies suggest abnormalities in limbic brain activity during emotional information processing in impulsively aggressive subjects with Intermittent Explosive Disorder (IED). It is not known if IED is associated with altered amygdala and hippocampus volume and shape.MethodsWe examined the volume and shape of the amygdala–hippocampal complex, using morphometric analysis of high resolution structural 3T MR scans in healthy control (HC: n = 73) subjects without history of Axis I or II psychiatric conditions and in subjects with IED (n = 67).ResultsWhile no volume differences were observed between HC and IED subjects, a significant level of morphometric deformation, suggestive of cell loss, in both amygdala and hippocampal structures was observed bilaterally in IED subjects. Analysis of a canonical variable that used the first 10 eigenvectors from both sides of the brain revealed that these morphometric deformations in the IED subjects were not due the presence of confounding variables or to comorbidities among IED subjects.ConclusionsThese data reveal that IED is associated with a significant loss of neurons in both the amygdala and hippocampus. These changes may play a role in the functional abnormalities observed in previous fMRI studies and in the pathophysiology of impulsive aggressive behavior.  相似文献   
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目的:探讨卒中后抑郁( post-stroke depression, PSD )大鼠前额叶皮质、海马和杏仁核中胶质纤维酸性蛋白(glial fibrilary acidic protein, GFAP)表达。方法健康成年SD大鼠随机分为正常组、抑郁组、卒中组和PSD组,每组5只。卒中组采用线栓法建立局灶性脑缺血模型;抑郁组采用慢性不可预见性温和应激(chronic unpredictable mild stress, CUMS )结合孤养建立大鼠慢性应激抑郁模型;PSD组采用线栓法建立局灶性脑缺血模型,术后1周加以CUMS 和孤养建立PSD 大鼠模型。在首次CUMS 后第1天、第8天、第15天和第29天进行蔗糖水消耗实验( sucrose preference test, SPT)和旷场实验(open-field test, OFT)评价抑郁行为,在第29天应用免疫荧光染色法检测前额叶皮质、海马和杏仁核GFAP表达。结果在CUMS后第29天时,抑郁组和PSD组SPT 蔗糖水消耗量以及OFT水平和垂直运动评分均显著低于正常组和卒中组(P均<0.05);PSD组前额叶皮质、海马和杏仁核GFAP免疫阳性细胞数量均显著少于正常组、抑郁组和卒中组(P均<0.05),而正常组、抑郁组和卒中组之间差异均无统计学意义( P均>0.05)。结论 PS D 大鼠前额叶皮质、海马和杏仁核GFAP表达下降可能在PSD发病过程中发挥着一定的作用。  相似文献   
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The amygdala, a crucial hub of the emotional processing neural system, has been implicated in late-life depression (LLD) pathophysiology. However, the overlapping and diverging amygdala network function abnormalities underlying two clinical LLD phenotypes (i.e., LLD alone and LLD with mild cognitive impairment [LLD-MCI]) are unknown. The aim of this study is to investigate the amygdala functional connectivity (FC) differences between LLD alone, LLD-MCI and healthy controls, and to examine the relationships between amygdala network dysfunction and symptom dimensions. A resting-state functional connectivity magnetic resonance imaging study was conducted to probe amygdala FC in a total of 63 elderly participants (LLD [n = 22], LLD-MCI [n = 15], and age- and gender-equated healthy older adults [n = 26]) using a seed-based voxelwise R-fcMRI approach. LLD-only adults showed increased FC in the posterior default mode and vermis, and diminished connections in the fronto-parietal, salience and temporal areas, relative to controls. The LLD-MCI participants showed diminished FC in the default mode, cognitive control, salience and visual regions, whereas increased FC was limited to lateral parietal cortex compared with healthy controls. The LLD-MCI group also showed diminished FC in the occipital and posterior default mode areas, relative to the LLD-only group. Distinct amygdala FC abnormalities that explain depressive and anxiety symptom severity, and executive functioning were identified. The amygdala FC impairments may distinguish LLD phenotypes. These functional network abnormalities may also explain the heterogeneity seen in the LLD clinical presentations.  相似文献   
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《Medical image analysis》2015,23(1):89-101
Image-based parcellation of the brain often leads to multiple disconnected anatomical structures, which pose significant challenges for analyses of morphological shapes. Existing shape models, such as the widely used spherical harmonic (SPHARM) representation, assume topological invariance, so are unable to simultaneously parameterize multiple disjoint structures. In such a situation, SPHARM has to be applied separately to each individual structure. We present a novel surface parameterization technique using 4D hyperspherical harmonics in representing multiple disjoint objects as a single analytic function, terming it HyperSPHARM. The underlying idea behind HyperSPHARM is to stereographically project an entire collection of disjoint 3D objects onto the 4D hypersphere and subsequently simultaneously parameterize them with the 4D hyperspherical harmonics. Hence, HyperSPHARM allows for a holistic treatment of multiple disjoint objects, unlike SPHARM. In an imaging dataset of healthy adult human brains, we apply HyperSPHARM to the hippocampi and amygdalae. The HyperSPHARM representations are employed as a data smoothing technique, while the HyperSPHARM coefficients are utilized in a support vector machine setting for object classification. HyperSPHARM yields nearly identical results as SPHARM, as will be shown in the paper. Its key advantage over SPHARM lies computationally; HyperSPHARM possess greater computational efficiency than SPHARM because it can parameterize multiple disjoint structures using much fewer basis functions and stereographic projection obviates SPHARM’s burdensome surface flattening. In addition, HyperSPHARM can handle any type of topology, unlike SPHARM, whose analysis is confined to topologically invariant structures.  相似文献   
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Activation of glucocorticoid receptor signaling in the stress response to traumatic events has been implicated in the pathogenesis of stress-associated psychiatric disorders such as post-traumatic stress disorder (PTSD). Elevated startle response and hyperarousal are hallmarks of PTSD, and are generally considered to evince fear (DSM V). To further examine the efficacy of corticosterone in treating hyperarousal and elevated fear, the present study utilized a learned helplessness stress model in which rats are restrained and subjected to tail shock for three days. These stressed rats develop a delayed long-lasting exaggeration of the acoustic startle response (ASR) and retarded body weight growth, similar to symptoms of PTSD patients (Myers et al., 2005; Speed et al., 1989). We demonstrate that both pre-stress and post-stress administration of corticosterone (3 mg/kg/day) mitigates a subsequent exaggeration of the ASR measured 14 days after cessation of the stress protocol. Furthermore, the mitigating efficacy of pre-stress administration of corticosterone (3 mg/kg/day for three days) appeared to last significantly longer, up to 21 days after the cessation of the stress protocol, in comparison to that of post-stress administration of corticosterone. However, pre-stress administration of corticosterone at 0.3 mg/kg/day for three days did not mitigate stress-induced exaggeration of the ASR measured at both 14 and 21 days after the cessation of the stress protocol. In addition, pre-stress administration of corticosterone (3 mg/kg/day for three days) mitigates the retardation of body weight growth otherwise resulting from the stress protocol. Congruently, co-administration of the corticosterone antagonist RU486 (40 mg/kg/day for three days) with corticosterone (3 mg/kg/day) prior to stress diminished the mitigating efficacy of the exogenous corticosterone on exaggerated ASR and stress-retarded body weight. The relative efficacy of pre versus post administration of corticosterone and high versus low dose of corticosterone on stress-induced exaggeration of innate fear response and stress-retarded body weight growth indicate that exogenous corticosterone administration within an appropriate time window and dosage are efficacious in diminishing traumatic stress induced pathophysiological processes. Clinical implications associated with the efficacy of prophylactic and therapeutic corticosterone therapy for mitigating symptoms of PTSD are discussed, particularly in relation to diminishing hyperarousal and exaggerated innate fear response.  相似文献   
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Background

Chronic stress exposure increases the risk of developing various neuropsychiatric illnesses. The behavioral sequelae of stress correlate with dendritic hypertrophy and glutamate-related synaptic remodeling at basolateral amygdala projection neurons (BLA PNs). Yet, though BLA PNs are functionally heterogeneous with diverse corticolimbic targets, it remains unclear whether stress differentially impacts specific output circuits.

Methods

Confocal imaging was used to reconstruct the morphology of mouse BLA PNs with the aid of retrograde tracing and biocytin staining. The synaptic activity in these neurons was measured with in vitro electrophysiology, and anxiety-like behavior of the mice was assessed with the elevated plus maze and open field test.

Results

Chronic restraint stress (CRS) produced dendritic hypertrophy across mouse BLA PNs, regardless of whether they did (BLA→dorsomedial prefrontal cortex [dmPFC]) or did not (BLA?dmPFC) target dmPFC. However, CRS increased the size of dendritic spine heads and the number of mature, mushroom-shaped spines only in BLA?dmPFC PNs, sparing neighboring BLA→dmPFC PNs. Moreover, the excitatory glutamatergic transmission was also selectively increased in BLA?dmPFC PNs, and this effect correlated with CRS-induced increases in anxiety-like behavior. Segregating BLA?dmPFC PNs based on their targeting of ventral hippocampus (BLA→ventral hippocampus) or nucleus accumbens (BLA→nucleus accumbens) revealed that CRS increased spine density and glutamatergic signaling in BLA→ventral hippocampus PNs in a manner that correlated with anxiety-like behavior.

Conclusions

Chronic stress caused BLA PN neuronal remodeling with a previously unrecognized degree of circuit specificity, offering new insight into the pathophysiological basis of depression, anxiety disorders, and other stress-related conditions.  相似文献   
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