scholarly journals Allergen-induced anxiety-like behavior is associated with disruption of medial prefrontal cortex - amygdala circuit

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Kolsoum Dehdar ◽  
Shirin Mahdidoust ◽  
Morteza Salimi ◽  
Leila Gholami-Mahtaj ◽  
Milad Nazari ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Allergic Inflammation ◽  
Poor Quality ◽  
Dynamic Interactions ◽  
Behavioral Expression ◽  
Amygdala Activity ◽  
Underlying Mechanisms ◽  
And Function ◽  
The Impact

AbstractAnxiety is prevalent in asthma, and is associated with disease severity and poor quality of life. However, no study to date provides direct experimental evidence for the effect of allergic inflammation on the structure and function of medial prefrontal cortex (mPFC) and amygdala, which are essential regions for modulating anxiety and its behavioral expression. We assessed the impact of ovalbumin (OVA)-induced allergic inflammation on the appearance of anxiety-like behavior, mPFC and amygdala volumes using MRI, and the mPFC-amygdala circuit activity in sensitized rats. Our findings exhibited that the OVA challenge in sensitized rats induced anxiety-like behavior, and led to more activated microglia and astrocytes in the mPFC and amygdala. We also found a negative correlation between anxiety-like behavior and amygdala volume. Moreover, OVA challenge in sensitized rats was associated with increases in mPFC and amygdala activity, elevation of amygdala delta-gamma coupling, and the enhancement of functional connectivity within mPFC-amygdala circuit – accompanied by an inverted direction of information transferred from the amygdala to the mPFC. We indicated that disrupting the dynamic interactions of the mPFC-amygdala circuit may contribute to the induction of anxiety-related behaviors with asthma. These findings could provide new insight to clarify the underlying mechanisms of allergic inflammation-induced psychiatric disorders related to asthma.

scholarly journals Estradiol Modulates Medial Prefrontal Cortex and Amygdala Activity During Fear Extinction in Women and Female Rats

2011 ◽  
Vol 70 (10) ◽  
pp. 920-927 ◽  
Author(s):  
Mohamed A. Zeidan ◽  
Sarah A. Igoe ◽  
Clas Linnman ◽  
Antonia Vitalo ◽  
John B. Levine ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Fear Extinction ◽  
Female Rats ◽  
Amygdala Activity

scholarly journals Behavioral control, the medial prefrontal cortex, and resilience

2006 ◽  
Vol 8 (4) ◽  
pp. 397-406 ◽  
Keyword(s):  
Prefrontal Cortex ◽  
Brain Stem ◽  
Medial Prefrontal Cortex ◽  
Behavioral Control ◽  
Initial Experience ◽  
Limbic Structures ◽  
Ventral Medial Prefrontal Cortex ◽  
The Face ◽  
Degree Of Control ◽  
The Impact

The degree of control that an organism has over a stressor potently modulates the impact of the stressor, with uncontrollable stressors producing a constellation of outcomes that do not occur if the stressor is behaviorally controllable. It has generally been assumed that this occurs because uncontrollability actively potentiates the effects of stressors. Here it will be suggested that in addition, or instead, the presence of control actively inhibits the impact of stressors. At least in part, this occurs because (i) the presence of control is detected by regions of the ventral medial prefrontal cortex (mPFCv); and (ii) detection of control activates mPFCv output to stress-responsive brain stem and limbic structures that actively inhibit stress-induced activation of these structures. Furthermore, an initial experience with control over stress alters the mPFCv response to subsequent stressors so that mPFCv output is activated even if the subsequent stressor is uncontrollable, thereby making the organism resilient. The general implications of these results for understanding resilience in the face of adversity are discussed.

scholarly journals Theta oscillations synchronize human medial prefrontal cortex and amygdala during fear learning

2021 ◽  
Vol 7 (34) ◽  
pp. eabf4198
Author(s):  
Si Chen ◽  
Zheng Tan ◽  
Wenran Xia ◽  
Carlos Alexandre Gomes ◽  
Xilei Zhang ◽  
...  
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Animal Studies ◽  
Theta Oscillations ◽  
Fear Learning ◽  
General Mechanism ◽  
Conditioning Paradigm ◽  
Amygdala Activity ◽  
Intracranial Electroencephalography ◽  
Patients With Epilepsy

Numerous animal studies have demonstrated that fear acquisition and expression rely on the coordinated activity of medial prefrontal cortex (mPFC) and amygdala and that theta oscillations support interregional communication within the fear network. However, it remains unclear whether these results can be generalized to fear learning in humans. We addressed this question using intracranial electroencephalography recordings in 13 patients with epilepsy during a fear conditioning paradigm. We observed increased power and inter-regional synchronization of amygdala and mPFC in theta (4 to 8 hertz) oscillations for conditioned stimulus (CS+) versus CS−. Analysis of information flow revealed that the dorsal mPFC (dmPFC) led amygdala activity in theta oscillations. Last, a computational model showed that trial-by-trial changes in amygdala theta oscillations predicted the model-based associability (i.e., learning rate). This study provides compelling evidence that theta oscillations within and between amygdala, ventral mPFC, and dmPFC constitute a general mechanism of fear learning across species.

scholarly journals “The Enemy of My Enemy is My Friend”: Shared Negative but not Positive Emotional Experience is Associated with Neural Synchrony in the Medial Prefrontal Cortex

2021 ◽  
Author(s):  
Jiani Li ◽  
MACRINA DIEFFENBACH ◽  
MATTHEW D. LIEBERMAN
Keyword(s):  
Prefrontal Cortex ◽  
Medial Prefrontal Cortex ◽  
Subjective Experience ◽  
Near Infrared ◽  
Emotional Experience ◽  
Human Life ◽  
Neural Synchrony ◽  
Functional Near Infrared Spectroscopy ◽  
Neural Signature ◽  
The Impact

Prevalent, automatic, and powerful, emotional experience forms an integral part of human life. Despite numerous studies pointing at the impact of emotion in shaping one’s interpretation of situation and guiding action, emotional experience has not been studied extensively due to its idiosyncratic nature. However, advances in neuroimaging techniques and statistical analysis methods enabled more rigorous investigation of subjective experience, one of which is neural synchrony. Here we sought to examine if neural synchrony in regions within the default mode network, including medial prefrontal cortex (mPFC), bilateral temporoparietal junctions (TPJ) and inferior parietal lobules (IPL), underlies shared emotional experience. A hundred and four participants watched political videos while being scanned by Functional Near-Infrared Spectroscopy (fNIRS) and rated their emotional experience afterwards. Although initial Inter- Subject Correlation Analysis and Inter-Subject Representational Similarity Analysis did not yield significant findings, we addressed limitations of both approaches – loss of dimensionality and unequal comparisons of dyads – by combining them with k-means clustering. This improved version of analysis revealed that subjects who reported more similarly negative, but not positive, emotional experiences exhibited more synchronized neural fluctuations in mPFC. The results suggest that neural synchrony in mPFC may be driven primarily by negative sentiments and serve as a neural signature for subjective emotional experience.

Exercise in Hypertrophic Cardiomyopathy: Restrict or Rethink??

2021 ◽  
Author(s):  
Adaya Weissler Snir ◽  
Kim A. Connelly ◽  
Jack M. Goodman ◽  
David Dorian ◽  
Paul Dorian
Keyword(s):  
Hypertrophic Cardiomyopathy ◽  
Animal Studies ◽  
Critical Evaluation ◽  
Sports Participation ◽  
Potential Benefits ◽  
Underlying Mechanisms ◽  
Exercise Induced ◽  
And Function ◽  
The Impact ◽  
Exercise Restriction

The detailed physiological consequences of aerobic training, in patients with hypertrophic cardiomyopathy (HCM) are not well understood. In athletes and non-athletes with HCM, there are two hypothetical concerns with respect to exercise: exercise-related worsening of the phenotype (e.g. promoting hypertrophy, fibrosis), and/or triggering of arrhythmia. The former concern is unproven and animal studies suggest an opposite effect, where exercise has been shown to be protective. The main reason for exercise restriction in HCM is fear of exercise-induced arrhythmia. Whilst the safety of sports in HCM has been reviewed, even more recent data suggest a substantially lower risk for sudden cardiac death (SCD) in HCM than previously thought, and there is an ongoing debate about restrictions of exercise imposed on individuals with HCM. This review outlines the pathophysiology of HCM, the impact of acute and chronic exercise (and variations of exercise intensity, modality, and athletic phenotype) in HCM including changes in autonomic function, blood pressure, cardiac dimensions and function, and cardiac output, and the underlying mechanisms that may trigger exercise-induced lethal arrhythmias. It provides a critical evaluation of the evidence regarding risk of SCD in athletes and the potential benefits of targeted exercise prescription in adults with HCM. Finally, it provides considerations for personalized recommendations for sports participation based on the available data.

scholarly journals Current understanding of cortical structure and function in migraine

Cephalalgia ◽  
2019 ◽  
Vol 39 (13) ◽  
pp. 1683-1699 ◽  
Author(s):  
Else A Tolner ◽  
Shih-Pin Chen ◽  
Katharina Eikermann-Haerter
Keyword(s):  
Structure And Function ◽  
Dynamic Interactions ◽  
Therapeutic Implications ◽  
Functional Changes ◽  
Cortical Structure ◽  
Modifying Factors ◽  
Subcortical Regions ◽  
Underlying Mechanisms ◽  
Cortical Regions ◽  
And Function

Objective To review and discuss the literature on the role of cortical structure and function in migraine. Discussion Structural and functional findings suggest that changes in cortical morphology and function contribute to migraine susceptibility by modulating dynamic interactions across cortical and subcortical networks. The involvement of the cortex in migraine is well established for the aura phase with the underlying phenomenon of cortical spreading depolarization, while increasing evidence suggests an important role for the cortex in perception of head pain and associated sensations. As part of trigeminovascular pain and sensory processing networks, cortical dysfunction is likely to also affect initiation of attacks. Conclusion Morphological and functional changes identified across cortical regions are likely to contribute to initiation, cyclic recurrence and chronification of migraine. Future studies are needed to address underlying mechanisms, including interactions between cortical and subcortical regions and effects of internal (e.g. genetics, gender) and external (e.g. sensory inputs, stress) modifying factors, as well as possible clinical and therapeutic implications.

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