Relevant bibliographies by topics / Amygdala

Academic literature on the topic 'Amygdala'

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Published: 4 June 2021
Last updated: 6 July 2024

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Journal articles on the topic "Amygdala"

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Staniloiu, Angelica, and Hans J. Markowitsch. "A rapprochement between emotion and cognition: Amygdala, emotion, and self-relevance in episodic-autobiographical memory." Behavioral and Brain Sciences 35, no. 3 (May 23, 2012): 164–66. http://dx.doi.org/10.1017/s0140525x11001543.

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AbstractLindquist et al. remark that not all fear instances lead to heightened amygdalar activity and, instead, point to roles of the amygdala in detecting “motivationally salient “or “emotionally impactful” stimuli. By reviewing research on the amygdala's functions in episodic-autobiographical memory, we further emphasize the involvement of the amygdala in coding the subjective relevance and extracting the biological and social significance of the stimuli.
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Nolan, Mark, Elena Roman, Anurag Nasa, Kirk J. Levins, Erik O’Hanlon, Veronica O’Keane, and Darren Willian Roddy. "Hippocampal and Amygdalar Volume Changes in Major Depressive Disorder: A Targeted Review and Focus on Stress." Chronic Stress 4 (January 2020): 247054702094455. http://dx.doi.org/10.1177/2470547020944553.

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Medial temporal lobe structures have long been implicated in the pathogenesis of major depressive disorder. Although findings of smaller hippocampal and amygdalar volumes are common, inconsistencies remain in the literature. In this targeted review, we examine recent and significant neuroimaging papers examining the volumes of these structures in major depressive disorder. A targeted PubMed/Google Scholar search was undertaken focusing on volumetric neuroimaging studies of the hippocampus and amygdala in major depressive disorder. Where possible, mean volumes and accompanying standard deviations were extracted allowing computation of Cohen’s ds effect sizes. Although not a meta-analysis, this allows a broad comparison of volume changes across studies. Thirty-nine studies in total were assessed. Hippocampal substructures and amygdale substructures were investigated in 11 and 2 studies, respectively. The hippocampus was more consistently smaller than the amygdala across studies, which is reflected in the larger cumulative difference in volume found with the Cohen’s ds calculations. The left and right hippocampi were, respectively, 92% and 91.3% of the volume found in controls, and the left and right amygdalae were, respectively, 94.8% and 92.6% of the volume of controls across all included studies. The role of stress in temporal lobe structure volume reduction in major depressive disorder is discussed.
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Tsai, Sheng-Feng, Hung-Tsung Wu, Pei-Chun Chen, Yun-Wen Chen, Megan Yu, Shun-Fen Tzeng, Pei-Hsuan Wu, Po-See Chen, and Yu-Min Kuo. "Stress Aggravates High-Fat-Diet-Induced Insulin Resistance via a Mechanism That Involves the Amygdala and Is Associated with Changes in Neuroplasticity." Neuroendocrinology 107, no. 2 (2018): 147–57. http://dx.doi.org/10.1159/000491018.

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Background: The notion that exposure to chronic stress predisposes individuals to developing type 2 diabetes (T2D) has gained much attention in recent decades. Long-term stress induces neuroadaptation in the amygdala and increases corticosterone levels. Corticosterone, the major stress hormone in rodents, induces insulin resistance and obesity in mice. However, little is known about whether the stress-induced amygdalar neuroadaptation could promote the risk of T2D. Methods: We used an 11-week high-fat diet (HFD) feeding paradigm to induce insulin dysfunction in mice, followed by implementation of a 10-day social defeat (SD) stress protocol. Results: Mice receiving SD at the beginning of the HFD feeding aggravated HFD-induced insulin resistance and white adipose tissue expansion. HFD mice had higher levels of plasma corticosterone, which was not affected by the SD. The SD stress upregulated the expression of TrkB and synaptotagmin-4 in the amygdala of HFD mice. Bilateral lesions of the central amygdalae before SD stress inhibited the stress-induced aggravating effect without affecting the HFD-induced elevation of plasma corticosterone. Conclusions: Stress aggravates HFD-induced insulin resistance and neuroadaptation in the amygdala. The HFD-induced insulin resistance is amygdala-dependent. Understanding the role of stress-induced amygdalar adaptation in the development of T2D could inform therapies aimed at reducing chronic stressors to decrease the risk for T2D.
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Oshri, Assaf, Joshua C. Gray, Max M. Owens, Sihong Liu, Erinn Bernstein Duprey, Lawrence H. Sweet, and James MacKillop. "Adverse Childhood Experiences and Amygdalar Reduction: High-Resolution Segmentation Reveals Associations With Subnuclei and Psychiatric Outcomes." Child Maltreatment 24, no. 4 (April 28, 2019): 400–410. http://dx.doi.org/10.1177/1077559519839491.

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The aim of the present study was 2-fold: (1) to utilize improved amygdala segmentation and exploratory factor analysis to characterize the latent volumetric structure among amygdala nuclei and (2) to assess the effect of adverse childhood experiences (ACEs) on amygdalar morphometry and current psychiatric symptoms. To investigate these aims, structural (T1) MRI and self-report data were obtained from 119 emerging adults. Regression analysis showed that higher ACE scores were related to reduced volume of the right, but not the left, amygdalar segments. Further, exploratory factor analysis yielded a two-factor structure, basolateral and central-medial nuclei of the right amygdala. Stractual equation modeling analyses revealed that higher ACE scores were significantly related to a reduced volume of the right basolateral and central-medial segments. Furthermore, reduction in the right basolateral amygdala was associated with increased anxiety, depressive symptoms, and alcohol use. This association supports an indirect effect between early adversity and psychiatric problems via reduced right basolateral amygdalar volume. The high-resolution segmentation results reveal a latent structure among amygdalar nuclei, which is consistent with prior work conducted in nonhuman mammals. These findings extend previous reports linking early adversity, right amygdala volume, and psychopathology.
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Tomasino, B., M. Bellani, C. Perlini, G. Rambaldelli, R. Cerini, M. Isola, M. Balestrieri, et al. "Altered microstructure integrity of the amygdala in schizophrenia: a bimodal MRI and DWI study." Psychological Medicine 41, no. 2 (May 12, 2010): 301–11. http://dx.doi.org/10.1017/s0033291710000875.

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BackgroundThe amygdala plays a central role in the fronto-limbic network involved in the processing of emotions. Structural and functional abnormalities of the amygdala have recently been found in schizophrenia, although there are still contradictory results about its reduced or preserved volumes.MethodIn order to address these contradictory findings and to further elucidate the possibly underlying pathophysiological process of the amygdala, we employed structural magnetic resonance imaging (MRI) and diffusion weighted imaging (DWI), exploring amygdalar volume and microstructural changes in 69 patients with schizophrenia and 72 matched healthy subjects, relating these indices to psychopathological measures.ResultsMeasuring water diffusivity, the apparent diffusion coefficients (ADCs) for the right amygdala were found to be significantly greater in patients with schizophrenia compared with healthy controls, with a trend for abnormally reduced volumes. Also, significant correlations between mood symptoms and amygdalar volumes were found in schizophrenia.ConclusionsWe therefore provide evidence that schizophrenia is associated with disrupted tissue organization of the right amygdala, despite partially preserved size, which may ultimately lead to abnormal emotional processing in schizophrenia. This result confirms the major role of the amygdala in the pathophysiology of schizophrenia and is discussed with respect to amygdalar structural and functional abnormalities found in patients suffering from this illness.
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Adolphs, Ralph, and Daniel Tranel. "Impaired Judgments of Sadness But Not Happiness Following Bilateral Amygdala Damage." Journal of Cognitive Neuroscience 16, no. 3 (April 2004): 453–62. http://dx.doi.org/10.1162/089892904322926782.

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Although the amygdala's role in processing facial expressions of fear has been well established, its role in the processing of other emotions is unclear. In particular, evidence for the amygdala's involvement in processing expressions of happiness and sadness remains controversial. To clarify this issue, we constructed a series of morphed stimuli whose emotional expression varied gradually from very faint to more pronounced. Five morphs each of sadness and happiness, as well as neutral faces, were shown to 27 subjects with unilateral amygdala damage and 5 with complete bilateral amygdala damage, whose data were compared to those from 12 braindamaged and 26 normal controls. Subjects were asked to rate the intensity and to label the stimuli. Subjects with unilateral amygdala damage performed very comparably to controls. By contrast, subjects with bilateral amygdala damage showed a specific impairment in rating sad faces, but performed normally in rating happy faces. Furthermore, subjects with right unilateral amygdala damage performed somewhat worse than subjects with left unilateral amygdala damage. The findings suggest that the amygdala's role in processing of emotional facial expressions encompasses multiple negatively valenced emotions, including fear and sadness.
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Knuepfer, M. M., A. Eismann, I. Schutze, H. Stumpf, and G. Stock. "Responses of single neurons in amygdala to interoceptive and exteroceptive stimuli in conscious cats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 268, no. 3 (March 1, 1995): R666—R675. http://dx.doi.org/10.1152/ajpregu.1995.268.3.r666.

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The amygdala is critical for behavioral arousal and must therefore integrate a wide variety of inputs. We examined sensory inputs and the degree of convergence to single neurons in the amygdala in conscious freely moving cats. A pressor stimulus elicited responses, predominantly inhibitory, in one-half of the amygdalar neurons tested. Most neurons in the central and basal nuclei responded to carotid chemoreceptor activation typically with an excitation. Almost one-half of all amygdalar neurons tested, particularly in the central nucleus, received orthodromic input from the locus ceruleus, the substantia nigra, and/or the contralateral central nucleus of the amygdala. Exteroceptive sensory stimulation with optic, acoustic, tactile, and olfactory stimuli elicited responses in 33, 55, 39, and 59% of amygdalar neurons, respectively. Two-thirds of the neurons tested with more than one external stimulus modality responded in the same manner to the various stimuli (usually excitation), demonstrating a convergence of exteroceptive stimuli on single amygdalar neurons, particularly in the basal nucleus. Spontaneous and induced behavioral arousal elicited responses in 92 and 86% of neurons, respectively. Most neurons responded to multimodal exteroceptive stimuli and behavioral arousal in the same manner. We suggest that amygdalar inputs are highly varied and, in many cases, relatively nonspecific and that the amygdala integrates a large number of external and internal sensory modalities to regulate autonomic and behavioral responsiveness to various stimuli.
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Luo, Wenting, Yue Zhang, Zhaoxian Yan, Xian Liu, Xiaoyan Hou, Weicui Chen, Yongsong Ye, Hui Li, and Bo Liu. "The Instant Effects of Continuous Transcutaneous Auricular Vagus Nerve Stimulation at Acupoints on the Functional Connectivity of Amygdala in Migraine without Aura: A Preliminary Study." Neural Plasticity 2020 (December 10, 2020): 1–13. http://dx.doi.org/10.1155/2020/8870589.

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Background. A growing body of evidence suggests that both auricular acupuncture and transcutaneous auricular vagus nerve stimulation (taVNS) can induce antinociception and relieve symptoms of migraine. However, their instant effects and central treatment mechanism remain unclear. Many studies proved that the amygdalae play a vital role not only in emotion modulation but also in pain processing. In this study, we investigated the modulation effects of continuous taVNS at acupoints on the FC of the bilateral amygdalae in MwoA. Methods. Thirty episodic migraineurs were recruited for the single-blind, crossover functional magnetic resonance imaging (fMRI) study. Each participant attended two kinds of eight-minute stimulations, taVNS and sham-taVNS (staVNS), separated by seven days in random order. Finally, 27 of them were included in the analysis of seed-to-voxel FC with the left/right amygdala as seeds. Results. Compared with staVNS, the FC decreased during taVNS between the left amygdala and left middle frontal gyrus (MFG), left dorsolateral superior frontal gyrus, right supplementary motor area (SMA), bilateral paracentral lobules, bilateral postcingulum gyrus, and right frontal superior medial gyrus, so did the FC of the right amygdala and left MFG. A significant positive correlation was observed between the FC of the left amygdala and right SMA and the frequency/total time of migraine attacks during the preceding four weeks. Conclusion. Continuous taVNS at acupoints can modulate the FC between the bilateral amygdalae and pain-related brain regions in MwoA, involving the limbic system, default mode network, and pain matrix, with obvious differences between the left amygdala and the right amygdala. The taVNS may produce treatment effects by modulating the abnormal FC of the amygdala and pain networks, possibly having the same central mechanism as auricular acupuncture.
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Perez-Diaz, Oscar, Daylín Góngora, José L. González-Mora, Katya Rubia, Alfonso Barrós-Loscertales, and Sergio Elías Hernández. "Enhanced amygdala–anterior cingulate white matter structural connectivity in Sahaja Yoga Meditators." PLOS ONE 19, no. 3 (March 28, 2024): e0301283. http://dx.doi.org/10.1371/journal.pone.0301283.

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Objective To study the white matter connections between anterior cingulate cortex, anterior insula and amygdala as key regions of the frontal-limbic network that have been related to meditation. Design Twenty experienced practitioners of Sahaja Yoga Meditation and twenty nonmeditators matched on age, gender and education level, were scanned using Diffusion Weighted Imaging, using a 3T scanner, and their white matter connectivity was compared using diffusion tensor imaging analyses. Results There were five white matter fiber paths in which meditators showed a larger number of tracts, two of them connecting the same area in both hemispheres: the left and right amygdalae and the left and right anterior insula; and the other three connecting left anterior cingulate with the right anterior insula, the right amygdala and the left amygdala. On the other hand, non-meditators showed larger number of tracts in two paths connecting the left anterior insula with the left amygdala, and the left anterior insula with the left anterior cingulate. Conclusions The study shows that long-term practice of Sahaja Yoga Meditation is associated with larger white matter tracts strengthening interhemispheric connections between limbic regions and connections between cingulo-amygdalar and cingulo-insular brain regions related to top-down attentional and emotional processes as well as between top-down control functions that could potentially be related to the witness state perceived through the state of mental silence promoted with this meditation. On the other hand, reduced connectivity strength in left anterior insula in the meditation group could be associated to reduced emotional processing affecting top-down processes.
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Wieser, Heinz Gregor. "Mesial temporal lobe epilepsy versus amygdalar epilepsy: Late seizure recurrence after initially successful amygdalotomy and regained seizure control following hippocampectomy." Epileptic Disorders 2, no. 3 (September 2000): 141–51. http://dx.doi.org/10.1684/j.1950-6945.2000.tb00374.x.

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ABSTRACT We summarise the concept of mesial temporal lobe epilepsy and the pros and cons in order to define amygdala epilepsy. We present a patient with stereotactically proven right amygdalar seizure onset, associated with fear and vegetative autonomic signs and symptoms as the most prominent clinical ictal features. Following a right stereotactic amygdalotomy, the patient experienced an 11‐year seizure‐free period. Similar, but not identical, semeiology of complex partial seizures then recurred. A right‐sided selective hippocampectomy and excision of the previously lesioned amygdala was performed. Except for 2 complex partial seizures associated with withdrawal of antiepileptic drugs, the patient remained seizure‐free 9.5 years. This case underscores the important role of the amygdala in generating the semiology, and raises several questions concerning the existence of “amygdalar epilepsy”. The 11‐year seizure‐free period following the stereotactic destruction of the amygdala is a strong argument for this notion. The late seizure recurrence requiring a second operation might, however, be seen as an argument for the important role of the hippocampal formation in the syndrome of mesial temporal lobe epilepsy even when the amygdala has been identified as the seizure onset zone. The role of stereotactic amygdalotomy is briefly reviewed.
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Dissertations / Theses on the topic "Amygdala"

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Samuelsen, Chad L. "Chemosensory processing in the amygdala." Tallahassee, Florida : Florida State University, 2009. http://etd.lib.fsu.edu/theses/available/etd-09212009-161414/.

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Thesis (Ph. D.)--Florida State University, 2009.
Advisor: Michael Meredith, Florida State University, College of Arts and Sciences, Dept. of Biological Science. Title and description from dissertation home page (viewed on May 4, 2010). Document formatted into pages; contains xv, 131 pages. Includes bibliographical references.
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Holahan, Matthew R. "Amygdala involvement in aversive conditioning." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=19529.

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Research over the past several decades has revealed that the amygdala is involved in aversive, or fear, conditioning. However, the precise nature of this involvement remains a matter of debate. One hypothesis suggests that disrupting amygdala function eliminates the storage of memories formed during aversive conditioning, eliminating the production of internal responses that alter the expression of observable behaviors. Alternatively, lesions or inactivation of the amygdala may impair the modulation of memories in other brain regions and disrupt the ability to perform certain observable behaviors. The experiments reported in the present thesis examined these arguments by making multiple behavioral measures during exposure to unconditioned (US) or conditioned (CS) aversive cues. Amygdala activity was inferred from changes in c-Fos protein expression or activity was temporarily suppressed with muscimol injections. The relationship between the behavioral measures and the role of the amygdala in producing them was examined. Amygdala neurons expressing the c-Fos protein tracked exposure to the US and CS but did not coincide with expression of freezing. Temporary inactivation of the amygdala with muscimol injections before presentation of the US or exposure to the CS attenuated the expression of freezing and active place avoidance; two incompatible behaviors. Finally, temporary inactivation of amygdala activity blocked freezing, place avoidance, and memory modulation produced by the same posttraining exposure to an aversive CS. Since amygdala activation alone was not sufficient to produce freezing and inactivation of the amygdala eliminated freezing, place avoidance, and memory modulation, the results cannot be interpreted as reflecting a direct role for the amygdala in production of observable behaviors. The results also preclude the idea that memory modulation is the only function of the amygdala. Rather, the results of all three studies suggest that the amygdala stores an aversive representation of the US which promotes the expression of various behaviors, possibly through the production of internal responses reflecting an aversive affective state.
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Kim, Joshua Ph D. Massachusetts Institute of Technology. "Amygdala circuits underlying valence-specific behaviors." Thesis, Massachusetts Institute of Technology, 2018. http://hdl.handle.net/1721.1/117881.

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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Biology, 2018.
Cataloged from PDF version of thesis.
Includes bibliographical references (pages 54-61).
Threatening and rewarding stimuli evoke a set of distinct stereotyped behaviors, which can be categorized as negative and positive valence-related behaviors, respectively. The stereotypic nature of negative and positive valence-related behaviors suggests that threatening and rewarding stimuli engage evolutionarily predetermined neural circuits in the brain. The amygdala is an important mammalian brain region that is activated by negative and positive stimuli and mediates negative and positive valence-related behaviors. The current prevailing circuit model of the amygdala mainly considers negative behaviors and only recently has cell-type specific models have been proposed. Hence, the substrates, genetically distinct neuronal populations, for negative and positive behaviors are not known. The work presented here describes a genetically-defined amygdala circuit model for negative and positive behaviors. Development of a genetic-based circuit model of the amygdala revealed anatomical and genetic circuit motifs that underlie that amygdala circuits that mediate valence-specific behaviors.
NIH Pre-Doctoral Training Grant T32GM007287 RIKEN Brain Science Institute
by Joshua Kim.
Ph. D.
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Corden, Benjamin. "The amygdala and social cognitive impairment." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1445396/.

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This thesis investigated the role of the amygdala in social cognition by examining variability in social-perceptual abilities within the normal population and via experiments with individuals who have Asperger's syndrome (AS). I found that a significant proportion of men from the general population had a fear recognition deficit akin to that seen in patients with bilateral amygdala lesion and that poor fear recognition was associated with poor theory of mind ability and with reduced activation of the amygdala and associated areas of the 'social brain'. Further experiments suggested a mechanism for these impairments - reduced fixation of the eye region of the face - similar to that exhibited by patient SM, who has suffered bilateral amygdala damage. Overall, I found that AS subjects also had a fear recognition deficit when compared with matched controls. However, there was great variability in responses, with scores ranging from normal to severely impaired. Again, an eyetracking experiment showed that low fear recognition was related to a reduced amount of time spent fixating the eyes. Informed by recent neurodevelopmental models of amygdala involvement in autistic- spectrum disorders, I conducted psychological, neurophysiological and neuroanatomical experiments in order to examine the cause of this failure to attend to the eyes in some AS subjects. As a whole, the findings support a 'hyper-active amygdala model', in which social stimuli induce an aversive level of arousal and so are avoided. I suggest that inattention to social stimuli, which could have a number of possible aetiologies, might be at the heart of a general route to social cognitive impairment, which could be shared by several distinct populations.
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McQueeny, Timothy. "Amygdala Morphometry in Adolescent Marijuana Users." University of Cincinnati / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1288378300.

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Ravi, Shankaran Raguram. "Survival, danger perception and the amygdala." Thesis, KTH, Skolan för teknik och hälsa (STH), 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-119586.

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Fear is an emotion expressed by a subject which is under a threat or danger to secure itself.  It causes the “Fight or Flight” sensation in the being which is under attack. In previous studies, it is found that amygdala is the central unit in brain for fear stimuli. Here we have done two different neuroscience studies on fear with ultra high field MRI. Case 1: With ultra high field MRI brain images we visualised that there is a faster and short pathway to amygdala. Fear stimuli activate the amygdale even when the images are shown for a very short time of 50ms with which conscious recognition is not possible. This shows brain reacts to fear even before we recognise it consciously. Case 2: We investigated the influence of low and high spatial frequency fearful images in amygdala because of the contradiction in some previous studies. We compared low, high and broad spatial frequency images of fearful averted gaze faces, snakes and objects and found both high and low spatial frequency fear images affect the amygdale in the similar manner.
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Lamirault, Charlotte. "Rôle de l’amygdale dans les symptômes émotionnels de la Maladie de Huntington : étude d’un modèle de rat transgénique, BACHD." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS003.

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La Maladie de Huntington (MH) est une pathologie génétique neurodégénérative, causée par un nombre anormalement élevé de répétitions du codon CAG dans le gène codant pour la protéine huntingtine (htt). A un stade pré-symptomatique (avant les symptômes moteurs), des troubles émotionnels sont souvent observés chez les patients MH, tels une agitation, une anxiété, une irritabilité ainsi qu’une tendance à la dépression, une apathie et une perte du contrôle émotionnel. Dans le but d’étudier la physiopathologie sous-jacentes aux (dys)fonctions émotionnelles de la MH, nous analysons le rôle de l’amygdale (en particulier le noyau central (CeA)). Cette structure est connue pour être impliquée dans la régulation du processus émotionnel et avoir un volume réduit ainsi qu’un grand nombre d’agrégats chez les patients et chez des modèles animaux transgéniques. Afin d’étudier les symptômes émotionnels de la MH, nous avons utilisé un modèle de rats transgéniques récent, les BACHD. Nos résultats montrent que ces animaux sont hyper-anxieux et hyper-réactifs face aux situations menaçantes à un stade précoce de la maladie. Ces rats BACHD présentent également un nombre élevé d’agrégats de grande taille augmentant en fonction de l’âge spécifiquement dans le CeA par rapport au noyau basolateral (BLA). De plus, la modulation pharmacologique du CeA entraine un effet comportemental différentiel chez les rats BACHD par rapport aux rats normaux, attestant d’un défaut fonctionnel de cette structure à un stade précoce de la maladie. Finalement, l’hyper-activité cellulaire observée dans le CeA (partie médiane) des rats BACHD pourrait expliquer l’hyper-réactivité émotionnelle de ces animaux et participer aux troubles émotionnels de la MH
Huntington’s disease (HD) is a genetic neurodegenerative disorder, caused by an expanded CAG repeat in the gene encoding the huntingtin protein. At the presymptomatic phase, before motor symptoms occur, psychiatric and emotional disorders are observed with high prevalence in HD patients. Agitation, anxiety and irritability are often described but also depression and/or apathy, associated with a lack of emotional control.In search of the pathophysiology underlying the emotional (dys)functions of HD, we studied the role of the amygdala (especially the central nucleus (CeA)). This structure is known to be involved in emotional regulation and has a reduced volume and a large number of aggregates in both patients and transgenic rat models. To study the emotional symptoms of HD we used a recent model of transgenic rats, BACHD. Our results show that these animals are hyper-anxious and hyper-reactive to threatening situations at an early stage of the disease. BACHD rats also have a high number of large aggregates, increasing with age, specifically in the CeA compared to the basolateral nucleus (BLA). In addition, pharmacological modulation of the CeA induce differential behavioral effects in BACHD rats compared to WT rats, evidencing a functional deficit of the structure at an early stage of the disease. Finally, the cellular hyper-activity observed in the CeA (medial part) of BACHD rats could account for the emotional hyper-reactivity of these animals and participate of emotional disorders of HD
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Jaime-Bustamante, Kean (Kean Willyams). "The amygdala in value-guided decision making." Thesis, Massachusetts Institute of Technology, 2017. http://hdl.handle.net/1721.1/114076.

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Thesis: Ph. D. in Neuroscience, Massachusetts Institute of Technology, Department of Brain and Cognitive Sciences, 2017.
Cataloged from PDF version of thesis.
Includes bibliographical references.
The amygdala is a structure well known for its role in fear and reward learning, but how these mechanisms are used for decision-making is not well understood. Decision-making involves the rapid updating of cue associations as well as the encoding of a value currency, both processes in which the amygdala has been implicated. In this thesis I develop a strategy to study value-guided decision making in rodents using an olfactory binary choice task. Using a logistic regression model, I show that the value of expected rewards is a strong influence on choice, and can bias perceptual decisions. In addition, I show that decisions are influenced by events in the near past, and a specific bias towards correct choices in the near past can be detected using this analysis. Using genetic targeting of a sub-population of amygdala neurons, I show that this population is required for the rapid learning of an olfactory decision making task. Using in-vivo calcium imaging of this population I show that these neurons are active during the inter-trial interval and modulated by choice history, suggesting a mechanism by which choice history can influence current decisions.
by Kean Jaime-Bustamante.
Ph. D. in Neuroscience
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Blake, Yvonne. "The role of the amygdala in dreaming." Master's thesis, University of Cape Town, 2014. http://hdl.handle.net/11427/12718.

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Includes bibliographical references.
Neuro-imaging studies have strongly implicated the basolateral amygdala in dreaming (e.g. Maquet et al., 1996). Various neuropsychological dream theorists (Domhoff, 2001; Hobson, Pace-Schott & Stickgold, 2000; Revonsuo, 2000) propose central roles for the amygdala in dreaming (particularly in the generation of dream affect); however, little empirical research on its function in dreaming exists. Urbach-Wiethe Disease (UWD) is a very rare genetic condition that can lead to calcifications in the medial temporal lobes. This study analysed 26 dream reports collected from eight adult UWD patients with fully calcified basolateral amygdalae bilaterally, and compared them to 58 dream reports collected from 17 matched controls. Dream affect and various other dream characteristics were examined. A number of significant results of small to moderate effect size were found. Notably, UWD patients’ dream reports had a significantly higher mean intensity of positive affect than controls’ dream reports, a significantly lower mean intensity of negative affect, a significantly higher mean intensity of PLAY, and a significantly lower mean intensity of RAGE. The UWD patients’ dream reports were also significantly more wish-fulfilling than the controls’ dream reports, were significantly less likely to be classified as nightmares, and had a significantly lower word count and narrative item count. These results are consistent with an extensive literature that implicates the basolateral amygdala in fear conditioning, emotional appraisal and in similar affective processes in waking life (e.g. LeDoux, 2003; Pessoa, 2010). The dream reports were also analysed for instances of threat and escape, as well as for approach and avoidance behaviour, in order to test some of the hypotheses central to Revonsuo’s (2000) threat simulation theory (TST) of dreaming. These analyses produced no significant results. Given that the amygdala is essential to Revonsuo’s (2000) conceptualisation of dreaming as an evolutionarily adaptive mechanism to safely simulate threat avoidance, these findings contradict some of TST’s central predictions. In general, these findings suggest that the average dream of persons with bilateral basolateral amygdalae damage is significantly simpler, more pleasant, less unpleasant, more wish-fulfilling and less likely to be a nightmare than the average control dream. As such, the dream reports of the UWD patients seem strikingly similar to the dreams of young children.
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Fällmark, Amanda. "Social anxiety disorder : Amygdala activation and connectivity." Thesis, Högskolan i Skövde, Institutionen för biovetenskap, 2021. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-20176.

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Social anxiety disorder (SAD) interferes with everyday life. It can, for instance, hinder careers, relationships, and leisure time. It is a common anxiety disorder that was neglected for decades. SAD individuals crave and fear social interactions simultaneously, leading to isolation in our highly social world. Therefore, research surrounding these kinds of disorders is essential. This systematic review has focused on the neural aspects and differences between SAD and healthy controls surrounding amygdala activation and connectivity. Functional magnetic resonance imaging (fMRI) studies conducted using social and emotional tasks were included. Findings include increased amygdala activation to fearful faces and words and a positive correlation between amygdala activation and symptom severity. Further, deficits in emotion regulation and a finding of gradual habituation have been found in SAD compared to healthy controls. Some limitations to this research are the small sample sizes used in the included articles and the use of both SAD and individuals with generalized SAD. The study is essential to assess future questions and directions regarding diagnosis, treatment, and understanding of SAD.
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Books on the topic "Amygdala"

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Koze, DJ. Amygdala. [Berlin, Germany]: Pampa Records, 2013.

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Gonaseelan, Kerosha. Amygdala: Roman. [Oslo]: Transit, 2009.

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Tickle your amygdala. Denver, CO: Brain Books and Music, 2012.

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1963-, Whalen Paul J., and Phelps Elizabeth A, eds. The human amygdala. New York: Guilford Press, 2009.

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P, Aggleton John, ed. The amygdala: A functional analysis. 2nd ed. Oxford, OX: Oxford University Press, 2000.

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Asan, Esther. The Catecholaminergic Innervation of the Rat Amygdala. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72085-7.

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Space and Value in the Primate Amygdala. [New York, N.Y.?]: [publisher not identified], 2014.

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The catecholaminergic innervation of the rat amygdala. Berlin: Springer, 1998.

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Stujenske, Joseph Matthew. Prefrontal-Amygdala Circuits Regulating Fear and Safety. [New York, N.Y.?]: [publisher not identified], 2016.

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Chʻen, Li. Effect of spinal double hemisections on amygdala-kindled convulsions. Ottawa: National Library of Canada, 1993.

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Book chapters on the topic "Amygdala"

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Ulfig, N. "Amygdala." In Advances in Anatomy Embryology and Cell Biology, 43–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-642-59425-0_7.

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McQuiston, Rory. "Amygdala." In Encyclopedia of Clinical Neuropsychology, 213–15. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-57111-9_291.

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Scherrmann, Jean-Michel, Kim Wolff, Christine A. Franco, Marc N. Potenza, Tayfun Uzbay, Lisiane Bizarro, David C. S. Roberts, et al. "Amygdala." In Encyclopedia of Psychopharmacology, 78. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_705.

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McQuiston, Rory. "Amygdala." In Encyclopedia of Clinical Neuropsychology, 1–3. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-56782-2_291-2.

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Silton, Nava R., and Ariel Brandwein. "Amygdala." In Encyclopedia of Child Behavior and Development, 87–88. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-0-387-79061-9_122.

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Kennedy, Daniel P., and Ralph Adolphs. "Amygdala." In Encyclopedia of Autism Spectrum Disorders, 146–51. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1698-3_544.

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Leonardis, Eric J. "Amygdala." In Encyclopedia of Animal Cognition and Behavior, 236–40. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-319-55065-7_1249.

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Matta, Richard, Elena Choleris, and Martin Kavaliers. "Amygdala." In Encyclopedia of Personality and Individual Differences, 142–45. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-24612-3_726.

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Matta, Richard, Elena Choleris, and Martin Kavaliers. "Amygdala." In Encyclopedia of Personality and Individual Differences, 1–4. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-28099-8_726-1.

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Leonardis, Eric J. "Amygdala." In Encyclopedia of Animal Cognition and Behavior, 1–5. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-47829-6_1249-1.

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Conference papers on the topic "Amygdala"

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Li, Guoshi, Gregory J. Quirk, and Satish S. Nair. "Regulation of Fear by Amygdala Intercalated Cells in a Network Model of Fear Acquisition and Extinction." In ASME 2008 Dynamic Systems and Control Conference. ASMEDC, 2008. http://dx.doi.org/10.1115/dscc2008-2403.

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A computational model of the fear circuit was developed to study regulation of fear by amygdala intercalated (ITC) neurons within the amygdala. A new biophysical model of an ITC neuron was developed first to capture its bistable behavior caused by an unusual slowly deinactivating current. An existing lateral amygdala network model was then extended into an overall fear circuit by adding ITC neurons, together with additional amygdaloid structures. Using a biophysical Hebbian learning rule for plastic synapses, the model successfully simulated the amygdala responses during acquisition, extinction, and recall of extinction in auditory fear conditioning. Results showed that fear could be regulated by the bistability of ITC neurons. The model also suggested additional sites for the storage fear and extinction memories.
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Tanaka, Yuichiro, and Hakaru Tamukoh. "Hardware Implementation of Brain-Inspired Amygdala Model." In 2019 IEEE International Symposium on Circuits and Systems (ISCAS). IEEE, 2019. http://dx.doi.org/10.1109/iscas.2019.8702430.

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Tantry, Evelyne, Joshua Ortiz-Guzman, and Benjamin Arenkiel. "The Impact of Acetylcholine on Basolateral Amygdala Macrocircuits." In 2019 Conference on Cognitive Computational Neuroscience. Brentwood, Tennessee, USA: Cognitive Computational Neuroscience, 2019. http://dx.doi.org/10.32470/ccn.2019.1383-0.

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HE, Wenjie, Haibing BU, Zhonglin LI, Bin YAN, Li TONG, and Linyuan WANG. "Amygdala-Prefrontal Connectivity Analysis of Decoding Human Emotion." In International Conference on Biological Engineering and Pharmacy 2016 (BEP 2016). Paris, France: Atlantis Press, 2017. http://dx.doi.org/10.2991/bep-16.2017.10.

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Tamburo, Robert, Greg Siegle, George Stetten, C. Cois, Ken Rockot, John Galeotti, Charles Reynolds, and Howard Aizenstein. "LOCALIZING AMYGDALA STRUCTURE DIFFERENCES IN LATE-LIFE DEPRESSION." In 2007 4th IEEE International Symposium on Biomedical Imaging: From Nano to Macro. IEEE, 2007. http://dx.doi.org/10.1109/isbi.2007.356858.

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Wang, Zexuan, Jiong Chen, Wenxi Yang, Sumita Gara, Frederick Xu, Junhao Wen, Christos Davatzikos, and Li Shen. "Shape analysis of amygdala atrophy using SPHARM-OT." In Image Processing, edited by Ivana Išgum and Olivier Colliot. SPIE, 2023. http://dx.doi.org/10.1117/12.2654399.

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Tanaka, Yuichiro, and Hakaru Tamukoh. "Live Demonstration: Hardware Implementation of Brain-Inspired Amygdala Model." In 2019 IEEE International Symposium on Circuits and Systems (ISCAS). IEEE, 2019. http://dx.doi.org/10.1109/iscas.2019.8702213.

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Herrmann, MJ, N. Siminski, S. Böhme, JBM Zeller, MPI Becker, M. Bruchmann, D. Hofmann, et al. "Time unpredictability increases BNST and amygdala activity during threat processing." In Abstracts of the 2nd Symposium of the Arbeitsgemeinschaft für Neuropsychopharmakologie und Pharmakopsychiatrie (AGNP) and Deutsche Gesellschaft für Biologische Psychiatrie (DGBP). Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3403025.

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FAST, K., E. FUJIWARA, C. GRUBICH, H. J. MARKOWITSCH, and M. HERRMANN. "ROLE OF THE AMYGDALA IN EMOTIONAL MEMORY: A CASE STUDY." In Proceedings of the International School of Biocybernetics. WORLD SCIENTIFIC, 2002. http://dx.doi.org/10.1142/9789812776563_0035.

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Glickert, Greg, Ben Latimer, Pankaj Sah, and Satish S. Nair. "Reverse engineering information processing in lateral amygdala during auditory tones." In 2023 11th International IEEE/EMBS Conference on Neural Engineering (NER). IEEE, 2023. http://dx.doi.org/10.1109/ner52421.2023.10123856.

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Reports on the topic "Amygdala"

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Li, He, Maria Braga, Chris Hough, Sean Manion, Xiaolong Jiang, Aiquin Chen, Eleanore H. Gamble, Preetha Abraham, and V> Anderjaska. Neuroplasticity and Calcium Signaling in Stressed Rat Amygdala. Fort Belvoir, VA: Defense Technical Information Center, February 2005. http://dx.doi.org/10.21236/ada435451.

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Sabit, Zafer, Hristina Nocheva, and Roman Tashev. Modulation of Nociception by Angiotensin II Type 1 Receptors Antagonist Losartan Infused into Amygdala of Rats with a Model of Depression. "Prof. Marin Drinov" Publishing House of Bulgarian Academy of Sciences, August 2019. http://dx.doi.org/10.7546/crabs.2019.08.15.

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Coyner, Jennifer L. Differential Expression of Phosphorylated Mitogen-Activated Protein Kinase (pMAPK) in the Lateral Amygdala of Mice Selectively Bred for High and Low Fear. Fort Belvoir, VA: Defense Technical Information Center, June 2013. http://dx.doi.org/10.21236/ad1012913.

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Morphett, Jane, Alexandra Whittaker, Amy Reichelt, and Mark Hutchinson. Perineuronal net structure as a non-cellular mechanism of affective state, a scoping review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, August 2021. http://dx.doi.org/10.37766/inplasy2021.8.0075.

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Is the perineuronal net structure within emotional processing brain regions associated with changes in affective state? The objective of this scoping review is to bring together the literature on human and animal studies which have measured perineuronal net structure in brain regions associated with emotional processing (such as but not limited to amygdala, hippocampus and prefrontal cortex). Perineuronal nets are a specialised form of condensed extracellular matrix that enwrap and protect neurons (Suttkus et al., 2016), regulate synaptic plasticity (Celio and Blumcke, 1994) and ion homeostasis (Morawski et al., 2015). Perineuronal nets are dynamic structures that are influenced by external and internal environmental shifts – for example, increasing in intensity and number in response to stressors (Blanco and Conant, 2021) and pharmacological agents (Riga et al., 2017). This review’s objective is to generate a compilation of existing knowledge regarding the structural changes of perineuronal nets in experimental studies that manipulate affective state, including those that alter environmental stressors. The outcomes will inform future research directions by elucidating non-cellular central nervous system mechanisms that underpin positive and negative emotional states. These methods may also be targets for manipulation to manage conditions of depression or promote wellbeing. Population: human and animal Condition: affective state as determined through validated behavioural assessment methods or established biomarkers. This includes both positive and negative affective states. Context: PNN structure, measuringPNNs.
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