Search results for "Amygdala"

showing 10 items of 169 documents

Single dose of l-dopa makes extinction memories context-independent and prevents the return of fear

2013

Traumatic events can engender persistent excessive fear responses to trauma reminders that may return even after successful treatment. Extinction, the laboratory analog of behavior therapy, does not erase conditioned fear memories but generates competing, fear-inhibitory "extinction memories" that, however, are tied to the context in which extinction occurred. Accordingly, a dominance of fear over extinction memory expression--and, thus, return of fear--is often observed if extinguished fear stimuli are encountered outside the extinction (therapy) context. We show that postextinction administration of the dopamine precursor L-dopa makes extinction memories context-independent, thus strongly…

AdultMaleVentromedial prefrontal cortexPrefrontal CortexContext (language use)AmygdalaDevelopmental psychologyExtinction PsychologicalLevodopaMiceMemorymedicineAnimalsHumansFear conditioningPrefrontal cortexFear processing in the brainMultidisciplinarysocial sciencesExtinction (psychology)FearMiddle AgedAmygdalahumanitiesMice Inbred C57BLmedicine.anatomical_structurePNAS PlusAnxietymedicine.symptomPsychologyNeuroscience
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Experimental and methodological factors affecting test-retest reliability of amygdala BOLD responses.

2018

Previous studies reported poor to fair test-retest reliability of amygdala BOLD responses to emotional stimuli. However, these findings are very heterogeneous across and within studies. The present study sought to systematically examine experimental and methodological factors that contribute to this heterogeneity. Forty-six young subjects were scanned twice with a mean test-retest interval of 7 weeks. We compared amygdala reliability across three tasks: A face-matching task, passive viewing of emotional faces, and passive viewing of emotional scenes. We also explored whether extraction of physiological noise can affect the stability of amygdala responses. We assessed test-retest reliability…

AdultMalemedicine.medical_specialtyDissociation (neuropsychology)Cognitive NeuroscienceMultidimensional assessmentExperimental and Cognitive PsychologyAudiologyEmotional processingbehavioral disciplines and activitiesAmygdala050105 experimental psychology03 medical and health sciencesYoung Adult0302 clinical medicineDevelopmental NeurosciencemedicineHumans0501 psychology and cognitive sciencesGroup levelBiological PsychiatryBrain MappingEndocrine and Autonomic SystemsGeneral Neuroscience05 social sciencesEmotional stimuliReproducibility of ResultsRepeatabilityAmygdalaMagnetic Resonance ImagingCommunication noiseAffectNeuropsychology and Physiological Psychologymedicine.anatomical_structurenervous systemNeurologyVisual PerceptionFemalePsychologyArtifactsFacial Recognitionpsychological phenomena and processes030217 neurology & neurosurgeryPsychophysiology
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Neural correlates of an attentional bias to health-threatening stimuli in individuals with pathological health anxiety

2017

Background: An attentional bias to health-threat stimuli is assumed to represent the primary pathogenetic factor for the development and maintenance of pathological health anxiety (PHA; formerly termed “hypochondriasis”). However, little is known about the neural basis of this attentional bias in individuals with PHA.Methods: A group of patients with PHA, a group of depressed patients and a healthy control group completed an emotional Stroop task with health-threat (body symptom and illness) words and neutral control words while undergoing functional MRI.Results: We included 33 patients with PHA, 28 depressed patients and 31 controls in our analyses. As reflected in reaction times, patients…

AdultMalemedicine.medical_specialtyEmotionschemical and pharmacologic phenomenaAudiologyAttentional biasBrain mappingAmygdalaArousalAttentional Bias03 medical and health sciences0302 clinical medicineddc:150Reaction TimemedicineHumansPharmacology (medical)PsychiatryBiological PsychiatryAnterior cingulate cortexBrain MappingBrainmedicine.diseaseAnxiety DisordersMagnetic Resonance Imaging030227 psychiatryPsychiatry and Mental healthmedicine.anatomical_structureReadingStroop TestVisual PerceptionAnxietyFemalemedicine.symptomPsychologyAttitude to Health030217 neurology & neurosurgeryAnxiety disorderResearch PaperStroop effectJournal of Psychiatry & Neuroscience
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Expression of PSA-NCAM and synaptic proteins in the amygdala of psychiatric disorder patients.

2011

Neuroimaging has revealed structural abnormalities in the amygdala of different psychiatric disorders. The polysialylated neural cell adhesion molecule (PSA-NCAM), a molecule related to neuronal structural plasticity, which expression is altered in schizophrenia, major depression and in animal models of these disorders, may participate in these changes. However, PSA-NCAM has not been studied in the human amygdala. To know whether its expression and that of presynaptic markers, was affected in psychiatric disorders, we have analyzed post-mortem sections from the Stanley Neuropathology Consortium, which includes controls, schizophrenia, bipolar and major depression patients. PSA-NCAM was expr…

AdultMalemedicine.medical_specialtyGlutamate decarboxylaseSynaptophysinNeural Cell Adhesion Molecule L1NeuropathologyAmygdalamental disordersNeuropilmedicineHumansBipolar disorderPsychiatryBiological PsychiatryAgedNeuronsbiologyGlutamate DecarboxylaseMood DisordersMiddle Agedmedicine.diseaseAmygdalaPsychiatry and Mental healthmedicine.anatomical_structurenervous systemGene Expression RegulationSchizophreniaPhosphopyruvate HydratasePostmortem ChangesVesicular Glutamate Transport Protein 1Synaptophysinbiology.proteinAcetylcholinesteraseSchizophreniaSialic AcidsNeural cell adhesion moleculeFemalePsychologyCalcium-Calmodulin-Dependent Protein Kinase Type 2NeuroscienceJournal of psychiatric research
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Effects of post-extinction l-DOPA administration on the spontaneous recovery and reinstatement of fear in a human fMRI study

2015

Relapse is a pertinent problem in the treatment of anxiety disorders. In the laboratory, relapse is modeled as return of conditioned fear responses after successful fear extinction and is explained by insufficient retrieval and/or expression of the fear-inhibitory extinction memory that is generated during extinction learning. We have shown in mice and humans that return of fear can be prevented by administration of a single dose of the dopamine precursor l-3,4-dihydroxyphenylalanine (l-DOPA) immediately after extinction. In mice, this effect could be attributed to an enhancement of extinction memory consolidation. In our human study, we could not exclude that l-DOPA might have acted by int…

AdultMalemedicine.medical_treatmentDopamine AgentsSpontaneous recoveryExposure therapyVentromedial prefrontal cortexAmygdalaFear-potentiated startleExtinction PsychologicalDevelopmental psychologyLevodopaRandom AllocationDouble-Blind MethodConditioning PsychologicalmedicineHumansPharmacology (medical)Fear conditioningBiological PsychiatryMemory ConsolidationPharmacologyFear processing in the brainBrain MappingPsychotropic DrugsBrainFearGalvanic Skin Responsesocial sciencesExtinction (psychology)Magnetic Resonance ImaginghumanitiesPsychiatry and Mental healthmedicine.anatomical_structureNeurologyVisual PerceptionNeurology (clinical)CuesPsychologyNeuroscienceEuropean Neuropsychopharmacology
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Excitability regulation in the dorsomedial prefrontal cortex during sustained instructed fear responses: a TMS-EEG study

2018

AbstractThreat detection is essential for protecting individuals from adverse situations, in which a network of amygdala, limbic regions and dorsomedial prefrontal cortex (dmPFC) regions are involved in fear processing. Excitability regulation in the dmPFC might be crucial for fear processing, while abnormal patterns could lead to mental illness. Notwithstanding, non-invasive paradigms to measure excitability regulation during fear processing in humans are missing. To address this challenge we adapted an approach for excitability characterization, combining electroencephalography (EEG) and transcranial magnetic stimulation (TMS) over the dmPFC during an instructed fear paradigm, to dynamica…

AdultMalemedicine.medical_treatmentPrefrontal Cortexlcsh:MedicineElectroencephalographyAmygdalaBrain mappingArticle050105 experimental psychologyYoung Adult03 medical and health sciences0302 clinical medicineDorsomedial Prefrontal Cortex ; Fear Paradigm ; TMS-evoked Potentials (TEPs) ; Fear Network ; Fear ProcessingHeart RateReaction TimemedicineHumans0501 psychology and cognitive scienceslcsh:ScienceEvoked PotentialsBrain MappingElectroshockMultidisciplinarymedicine.diagnostic_test05 social scienceslcsh:RHealthy subjectsStructural integrityElectroencephalographyFearDorsomedial prefrontal cortexTranscranial Magnetic StimulationTranscranial magnetic stimulationmedicine.anatomical_structureFemalelcsh:QPsychologyNeuroscience030217 neurology & neurosurgery
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Neural correlates of antinociception in borderline personality disorder.

2006

Context A characteristic feature of borderline personality disorder (BPD) is self-injurious behavior in conjunction with stress-induced reduction of pain perception. Reduced pain sensitivity has been experimentally confirmed in patients with BPD, but the neural correlates of antinociceptive mechanisms in BPD are unknown. We predicted that heat stimuli in patients with BPD would activate brain areas concerned with cognitive and emotional evaluation of pain. Objective To assess the psychophysical properties and neural correlates of altered pain processing in patients with BPD. Design Case-control study. Setting A university hospital. Participants Twelve women with BPD and self-injurious behav…

AdultPain Thresholdmedicine.medical_specialtyHot TemperatureDifferential ThresholdPainPrefrontal CortexAudiologybehavioral disciplines and activitiesAmygdalaGyrus CingulimethodsArts and Humanities (miscellaneous)bloodBorderline Personality DisorderPhysical StimulationAdult Amygdala; physiopathology Borderline Personality Disorder; diagnosis/physiopathology/psychology Brain Mapping Brain; physiopathology Case-Control Studies Differential Threshold; physiology Female Gyrus Cinguli; physiopathology Hot Temperature; diagnostic use Humans Magnetic Resonance Imaging Oxygen; blood Pain Measurement; methods Pain Threshold; physiology Pain; diagnosis/physiopathology/psychology Physical Stimulation Prefrontal Cortex; physiopathology Self-Injurious Behavior; diagnosis/physiopathology Thermosensing; physiologymental disordersThreshold of painmedicineHumansThermosensingPrefrontal cortexPsychiatryBorderline personality disorderPain MeasurementBrain MappingBlood-oxygen-level dependentmedicine.diagnostic_testBrainmedicine.diseaseAmygdalaMagnetic Resonance Imagingdiagnosis/physiopathologyFunctional imagingDorsolateral prefrontal cortexOxygenPsychiatry and Mental healthmedicine.anatomical_structureCase-Control StudiesphysiologyFemalediagnosis/physiopathology/psychologyphysiopathologydiagnostic useFunctional magnetic resonance imagingPsychologySelf-Injurious BehaviorArchives of general psychiatry
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Alterations in the expression of PSA-NCAM and synaptic proteins in the dorsolateral prefrontal cortex of psychiatric disorder patients.

2012

Alterations in the structure and physiology of the prefrontal cortex (PFC) have been found in different psychiatric disorders and some of them involve inhibitory networks, especially in schizophrenia and major depression. Changes in the structure of these networks may be mediated by the polysialylated neural cell adhesion molecule (PSA-NCAM), a molecule related to neuronal structural plasticity, expressed in the PFC exclusively by interneurons. Different studies have found that PSA-NCAM expression in the hippocampus and the amygdala is altered in schizophrenia, major depression and animal models of these disorders, in parallel to changes in the expression of molecules related to inhibitory …

Adultmedicine.medical_specialtyBipolar DisorderSynaptophysinHippocampusPrefrontal CortexNeural Cell Adhesion Molecule L1NeurotransmissionHippocampusmedicineNeuropilHumansPsychiatryPrefrontal cortexAgedDepressive Disorder MajorNeuronal PlasticitybiologyGlutamate DecarboxylaseGeneral NeuroscienceMental DisordersNeural InhibitionMiddle AgedAmygdalaDorsolateral prefrontal cortexmedicine.anatomical_structurenervous systemSynaptic plasticitySynapsesVesicular Glutamate Transport Protein 1Synaptophysinbiology.proteinSchizophreniaSialic AcidsNeural cell adhesion moleculePsychologyNeuroscienceNeuroscience letters
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CB1 cannabinoid receptor-mediated aggressive behavior

2013

This study examined the role of cannabinoid CB1 receptors (CB1r) in aggressive behavior. Social encounters took place in grouped and isolated mice lacking CB1r (CB1KO) and in wild-type (WT) littermates. Cognitive impulsivity was evaluated in the delayed reinforcement task (DRT). Gene expression analyses of monoaminooxidase-A (MAO-A), catechol-o-methyl-transferase (COMT), 5-hydroxytriptamine transporter (5-HTT) and 5-HT1B serotonergic receptor (5HT1Br) in the median and dorsal raphe nuclei (MnR and DR, respectively) and in the amygdala (AMY) were performed by real time-PCR. Double immunohistochemistry studies evaluated COMT and CB1r co-localization in the raphe nuclei and in the cortical (AC…

AgonistMalemedicine.medical_specialtyCannabinoid receptorTime Factorsmedicine.drug_classmedicine.medical_treatmentPoison controlArachidonic AcidsSerotonergicCatechol O-MethyltransferaseAmygdalaCellular and Molecular NeuroscienceMiceDorsal raphe nucleusReceptor Cannabinoid CB1Internal medicinemedicineAnimalsInterpersonal RelationsMonoamine OxidasePharmacologyCannabinoid Receptor AgonistsMice KnockoutSerotonin Plasma Membrane Transport ProteinsAmygdalaSurgeryAggressionmedicine.anatomical_structureEndocrinologynervous systemGene Expression RegulationImpulsive BehaviorReceptor Serotonin 5-HT1BConditioning OperantRaphe NucleiCannabinoidRaphe nucleiPsychologyReinforcement Psychology
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Selective erasure of a fear memory

2009

International audience; Memories are thought to be encoded by sparsely distributed groups of neurons. However, identifying the precise neurons supporting a given memory (the memory trace) has been a long-standing challenge. We have shown previously that lateral amygdala (LA) neurons with increased cyclic adenosine monophosphate response element-binding protein (CREB) are preferentially activated by fear memory expression, which suggests that they are selectively recruited into the memory trace. We used an inducible diphtheria-toxin strategy to specifically ablate these neurons. Selectively deleting neurons overexpressing CREB (but not a similar portion of random LA neurons) after learning b…

AmnesiaApoptosisMice TransgenicCREBAmygdalaMice03 medical and health sciences0302 clinical medicineMemoryConditioning PsychologicalmedicineAnimalsMemory disorderCyclic AMP Response Element-Binding ProteinNeuronal memory allocation030304 developmental biologyMemory consolidation0303 health sciencesMultidisciplinarybiologyCREBMemoriaFearmedicine.diseaseAmygdalamedicine.anatomical_structurenervous systemMental Recallbiology.proteinMemory traceMemory consolidation[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]AmnesiaNeuronPavlovian conditioningmedicine.symptomNeuroscience030217 neurology & neurosurgeryScience
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