18 results on '"Cannon EN"'
Search Results
2. High-Fat Diet Augments Myocardial Inflammation and Cardiac Dysfunction in Arrhythmogenic Cardiomyopathy.
- Author
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Centner AM, Shiel EA, Farra W, Cannon EN, Landim-Vieira M, Salazar G, and Chelko SP
- Subjects
- Animals, Mice, Disease Models, Animal, Myocardium pathology, Myocardium metabolism, Fibrosis, Male, Ventricular Remodeling, Desmoglein 2 genetics, Myocarditis etiology, Myocarditis physiopathology, Mice, Inbred C57BL, Arrhythmogenic Right Ventricular Dysplasia etiology, Arrhythmogenic Right Ventricular Dysplasia physiopathology, Adiponectin blood, Inflammation, Cardiomyopathies etiology, Cardiomyopathies physiopathology, Diet, High-Fat adverse effects
- Abstract
Arrhythmogenic cardiomyopathy (ACM) is a familial heart disease characterized by cardiac dysfunction, arrhythmias, and myocardial inflammation. Exercise and stress can influence the disease's progression. Thus, an investigation of whether a high-fat diet (HFD) contributes to ACM pathogenesis is warranted. In a robust ACM mouse model, 8-week-old Desmoglein-2 mutant ( Dsg2
mut/mut ) mice were fed either an HFD or rodent chow for 8 weeks. Chow-fed wildtype (WT) mice served as controls. Echo- and electrocardiography images pre- and post-dietary intervention were obtained, and the lipid burden, inflammatory markers, and myocardial fibrosis were assessed at the study endpoint. HFD-fed Dsg2mut/mut mice showed numerous P-wave perturbations, reduced R-amplitude, left ventricle (LV) remodeling, and reduced ejection fraction (%LVEF). Notable elevations in plasma high-density lipoprotein (HDL) were observed, which correlated with the %LVEF. The myocardial inflammatory adipokines, adiponectin (AdipoQ) and fibroblast growth factor-1, were substantially elevated in HFD-fed Dsg2mut/mut mice, albeit no compounding effect was observed in cardiac fibrosis. The HFD not only potentiated cardiac dysfunction but additionally promoted adverse cardiac remodeling. Further investigation is warranted, particularly given elevated AdipoQ levels and the positive correlation of HDL with the %LVEF, which may suggest a protective effect. Altogether, the HFD worsened some, but not all, disease phenotypes in Dsg2mut/mut mice. Notwithstanding, diet may be a modifiable environmental factor in ACM disease progression.- Published
- 2024
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3. NFĸB signaling drives myocardial injury via CCR2+ macrophages in a preclinical model of arrhythmogenic cardiomyopathy.
- Author
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Chelko SP, Penna VR, Engel M, Shiel EA, Centner AM, Farra W, Cannon EN, Landim-Vieira M, Schaible N, Lavine K, and Saffitz JE
- Subjects
- Animals, Mice, Myocytes, Cardiac metabolism, Myocytes, Cardiac pathology, Myocytes, Cardiac immunology, Humans, Arrhythmogenic Right Ventricular Dysplasia genetics, Arrhythmogenic Right Ventricular Dysplasia metabolism, Arrhythmogenic Right Ventricular Dysplasia pathology, Myocardium pathology, Myocardium metabolism, Myocardium immunology, Macrophages metabolism, Macrophages pathology, Macrophages immunology, Receptors, CCR2 genetics, Receptors, CCR2 metabolism, Signal Transduction, Disease Models, Animal, Desmoglein 2 genetics, Desmoglein 2 metabolism, NF-kappa B metabolism, NF-kappa B genetics
- Abstract
Nuclear factor κ-B (NFκB) is activated in iPSC-cardiac myocytes from patients with arrhythmogenic cardiomyopathy (ACM) under basal conditions, and inhibition of NFκB signaling prevents disease in Dsg2mut/mut mice, a robust mouse model of ACM. Here, we used genetic approaches and single-cell RNA-Seq to define the contributions of immune signaling in cardiac myocytes and macrophages in the natural progression of ACM using Dsg2mut/mut mice. We found that NFκB signaling in cardiac myocytes drives myocardial injury, contractile dysfunction, and arrhythmias in Dsg2mut/mut mice. NFκB signaling in cardiac myocytes mobilizes macrophages expressing C-C motif chemokine receptor-2 (CCR2+ cells) to affected areas within the heart, where they mediate myocardial injury and arrhythmias. Contractile dysfunction in Dsg2mut/mut mice is caused both by loss of heart muscle and negative inotropic effects of inflammation in viable muscle. Single nucleus RNA-Seq and cellular indexing of transcriptomes and epitomes (CITE-Seq) studies revealed marked proinflammatory changes in gene expression and the cellular landscape in hearts of Dsg2mut/mut mice involving cardiac myocytes, fibroblasts, and CCR2+ macrophages. Changes in gene expression in cardiac myocytes and fibroblasts in Dsg2mut/mut mice were dependent on CCR2+ macrophage recruitment to the heart. These results highlight complex mechanisms of immune injury and regulatory crosstalk between cardiac myocytes, inflammatory cells, and fibroblasts in the pathogenesis of ACM.
- Published
- 2024
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4. Mechanisms of Innate Immune Injury in Arrhythmogenic Cardiomyopathy.
- Author
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Chelko SP, Penna V, Engel M, Landim-Vieira M, Cannon EN, Lavine K, and Saffitz JE
- Abstract
Inhibition of nuclear factor kappa-B (NFκB) signaling prevents disease in Dsg2
mut/mut mice, a model of arrhythmogenic cardiomyopathy (ACM). Moreover, NFκB is activated in ACM patient-derived iPSC-cardiac myocytes under basal conditions in vitro . Here, we used genetic approaches and sequencing studies to define the relative pathogenic roles of immune signaling in cardiac myocytes vs. inflammatory cells in Dsg2mut/mut mice. We found that NFκB signaling in cardiac myocytes drives myocardial injury, contractile dysfunction, and arrhythmias in Dsg2mut/mut mice. It does this by mobilizing cells expressing C-C motif chemokine receptor-2 (CCR2+ cells) to the heart, where they mediate myocardial injury and arrhythmias. Contractile dysfunction in Dsg2mut/mut mice is caused both by loss of heart muscle and negative inotropic effects of inflammation in viable muscle. Single nucleus RNA sequencing and cellular indexing of transcriptomes and epitomes (CITE-seq) studies revealed marked pro-inflammatory changes in gene expression and the cellular landscape in hearts of Dsg2mut/mut mice involving cardiac myocytes, fibroblasts and CCR2+ cells. Changes in gene expression in cardiac myocytes and fibroblasts in Dsg2mut/mut mice were modulated by actions of CCR2+ cells. These results highlight complex mechanisms of immune injury and regulatory crosstalk between cardiac myocytes, inflammatory cells, and fibroblasts in the pathogenesis of ACM., Brief Summary: We have uncovered a therapeutically targetable innate immune mechanism regulating myocardial injury and cardiac function in a clinically relevant mouse model of Arrhythmogenic Cardiomyopathy (ACM).- Published
- 2023
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5. Efficacy and Safety of Angiotensin Receptor Blockers in a Pre-Clinical Model of Arrhythmogenic Cardiomyopathy.
- Author
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Landim-Vieira M, Kahmini AR, Engel M, Cannon EN, Amat-Alarcon N, Judge DP, Pinto JR, and Chelko SP
- Subjects
- Animals, Mice, Angiotensin Receptor Antagonists pharmacology, Angiotensin Receptor Antagonists therapeutic use, Cicatrix, PPAR alpha, Rosiglitazone, Telmisartan pharmacology, Cardiomyopathies etiology, Cardiomyopathies genetics, Heart Diseases
- Abstract
Arrhythmogenic Cardiomyopathy (ACM) is a familial heart disease, characterized by contractile dysfunction, ventricular arrhythmias (VAs), and the risk of sudden cardiac death. Currently, implantable cardioverter defibrillators and antiarrhythmics are the mainstays in ACM therapeutics. Angiotensin receptor blockers (ARBs) have been highlighted in the treatment of heart diseases, including ACM. Yet, recent research has additionally implicated ARBs in the genesis of VAs and myocardial lipolysis via the peroxisome proliferator-activated receptor gamma (PPARγ) pathway. The latter is of particular interest, as fibrofatty infiltration is a pathological hallmark in ACM. Here, we tested two ARBs, Valsartan and Telmisartan, and the PPAR agonist, Rosiglitazone, in an animal model of ACM, homozygous Desmoglein-2 mutant mice ( Dsg2
mut/mut ). Cardiac function, premature ventricular contractions (PVCs), fibrofatty scars, PPARα/γ protein levels, and PPAR-mediated mRNA transcripts were assessed. Of note, not a single mouse treated with Rosiglitazone made it to the study endpoint (i.e., 100% mortality: n = 5/5). Telmisartan-treated Dsg2mut/mut mice displayed the preservation of contractile function (percent ejection fraction [%EF]; 74.8 ± 6.8%EF) compared to Vehicle- (42.5 ± 5.6%EF) and Valsartan-treated (63.1 ± 4.4%EF) mice. However, Telmisartan-treated Dsg2mut/mut mice showed increased cardiac wall motion abnormalities, augmented %PVCs, electrocardiographic repolarization/depolarization abnormalities, larger fibrotic lesions, and increased expression of PPARy-regulated gene transcripts compared to their Dsg2mut/mut counterparts. Alternatively, Valsartan-treated Dsg2mut/mut mice harbored fewer myocardial scars, reduced %PVC, and increased Wnt-mediated transcripts. Considering our findings, caution should be taken by physicians when prescribing medications that may increase PPARy signaling in patients with ACM.- Published
- 2022
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6. Transgenerational transmission of behavioral phenotypes produced by exposure of male mice to saccharin and nicotine.
- Author
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McCarthy DM, Lowe SE, Morgan TJ, Cannon EN, Biederman J, Spencer TJ, and Bhide PG
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- Animals, Body Weight drug effects, Crosses, Genetic, DNA Methylation drug effects, DNA Methylation genetics, Drinking Behavior drug effects, Female, Male, Methylphenidate pharmacology, Mice, Inbred C57BL, Motor Activity drug effects, Phenotype, Spermatozoa drug effects, Spermatozoa metabolism, Behavior, Animal drug effects, Nicotine pharmacology, Saccharin pharmacology
- Abstract
The use of non-nutritive sweeteners such as saccharin is widely prevalent. Although saccharin is considered safe for human consumption, it produces behavioral changes in experimental animals. We report that saccharin's behavioral effects are much more pervasive than currently recognized. In a mouse model, saccharin exposure produced motor impulsivity not only in the saccharin-exposed males but also in their offspring. In addition, the offspring showed locomotor hyperactivity and working memory deficit not observed in fathers. Spermatazoal DNA was hypermethylated in the saccharin-exposed fathers, especially at dopamine receptor promoter regions, suggesting that epigenetic modification of germ cell DNA may mediate transgenerational transmission of behavioral phenotypes. Dopamine's role in hyperactivity was further highlighted by the finding that the stimulant drug methylphenidate mitigated the hyperactivity. Nicotine is another substance that is widely used. Its use via smokeless tobacco products, some of which contain saccharin, is on the rise contributing to concerns about adverse outcomes of co-exposure to saccharin and nicotine. We found that co-exposure of male mice to saccharin and nicotine produced significant behavioral impairment in their offspring. Thus, our data point to potential adverse neurobehavioral consequences of exposure to saccharin alone or saccharin and nicotine for the exposed individuals and their descendants.
- Published
- 2020
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7. Supporting Infant Emotion Regulation Through Attachment-Based Intervention: a Randomized Controlled Trial.
- Author
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Hepworth AD, Berlin LJ, Martoccio TL, Cannon EN, Berger RH, and Harden BJ
- Subjects
- Adult, Early Intervention, Educational, Female, Hispanic or Latino, Humans, Infant, Infant Behavior psychology, Observation, Emotional Regulation, Mother-Child Relations ethnology, Object Attachment
- Abstract
Infant emotion regulation has long-term implications for human development, highlighting the need for preventive interventions that support emotion regulation early in life. Such interventions may be especially important for infants higher in emotional reactivity who need to regulate their emotions more frequently and intensely than infants lower in emotional reactivity. The current randomized trial examined main and moderated effects of an attachment-based intervention on (a) infants' use of mother-oriented and self-soothing emotion regulation strategies and (b) infant emotion dysregulation in 186 low-income, predominantly Latino infants. We tested the brief (10-session) Attachment and Biobehavioral Catch-up (ABC) intervention in the context of home-based federal Early Head Start (EHS) services. Control participants received home-based EHS plus 10 weekly books. Intent-to-treat analyses with covariates revealed main effects of the intervention on infants' use of mother-oriented emotion regulation strategies during a brief (40-s) novel and potentially fear-inducing procedure (d = 0.31). Infant emotional reactivity moderated intervention impacts on mother-oriented emotion regulation strategies and on infant emotion dysregulation: We found stronger effects of the intervention for infants relatively higher in emotional reactivity. Findings are discussed in terms of the preventive value of attachment-based interventions for supporting early emotion regulation.
- Published
- 2020
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8. The mu-rhythm can mirror: Insights from experimental design, and looking past the controversy.
- Author
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Bowman LC, Bakermans-Kranenburg MJ, Yoo KH, Cannon EN, Vanderwert RE, Ferrari PF, van IJzendoorn MH, and Fox NA
- Subjects
- Brain Waves, Electroencephalography, Mirror Neurons, Research Design
- Published
- 2017
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9. Action mechanisms for social cognition: behavioral and neural correlates of developing Theory of Mind.
- Author
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Bowman LC, Thorpe SG, Cannon EN, and Fox NA
- Subjects
- Age Factors, Brain Waves physiology, Child, Preschool, Electroencephalography, Female, Hand Strength physiology, Humans, Individuality, Male, Neuropsychological Tests, Verbal Behavior, Brain Mapping, Child Development, Cognition physiology, Motor Skills physiology, Social Behavior, Theory of Mind physiology
- Abstract
Many psychological theories posit foundational links between two fundamental constructs: (1) our ability to produce, perceive, and represent action; and (2) our ability to understand the meaning and motivation behind the action (i.e. Theory of Mind; ToM). This position is contentious, however, and long-standing competing theories of social-cognitive development debate roles for basic action-processing in ToM. Developmental research is key to investigating these hypotheses, but whether individual differences in neural and behavioral measures of motor action relate to social-cognitive development is unknown. We examined 3- to 5-year-old children's (N = 26) EEG mu-desynchronization during production of object-directed action, and explored associations between mu-desynchronization and children's behavioral motor skills, behavioral action-representation abilities, and behavioral ToM. For children with high (but not low) mu-desynchronization, motor skill related to action-representation abilities, and action-representation mediated relations between motor skill and ToM. Results demonstrate novel foundational links between action-processing and ToM, suggesting that basic motor action may be a key mechanism for social-cognitive development, thus shedding light on the origins and emergence of higher social cognition., (© 2016 John Wiley & Sons Ltd.)
- Published
- 2017
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10. A prenatal nicotine exposure mouse model of methylphenidate responsive ADHD-associated cognitive phenotypes.
- Author
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Zhu J, Fan F, McCarthy DM, Zhang L, Cannon EN, Spencer TJ, Biederman J, and Bhide PG
- Subjects
- Age Factors, Analysis of Variance, Animals, Animals, Newborn, Attention Deficit Disorder with Hyperactivity etiology, Drinking drug effects, Escape Reaction drug effects, Female, Litter Size drug effects, Male, Maze Learning drug effects, Mice, Mice, Inbred C57BL, Nicotine toxicity, Nicotinic Agonists toxicity, Pregnancy drug effects, Prenatal Exposure Delayed Effects chemically induced, Recognition, Psychology drug effects, Sex Factors, Attention Deficit Disorder with Hyperactivity complications, Central Nervous System Stimulants therapeutic use, Cognition Disorders drug therapy, Cognition Disorders etiology, Methylphenidate therapeutic use, Prenatal Exposure Delayed Effects physiopathology
- Abstract
Prenatal exposure to nicotine via cigarette smoke or other forms of tobacco use is a significant environmental risk factor for attention deficit hyperactivity disorder (ADHD). The neurobiological mechanisms underlying the link between prenatal nicotine exposure (PNE) and ADHD are not well understood. Animal models, especially rodent models, are beginning to bridge this gap in knowledge. Although ADHD is characterized by hyperactivity, inattention, impulsivity and working memory deficits, the majority of the animal models are based on only one or two ADHD associated phenotypes, in particular, hyperactivity or inattention. We report a PNE mouse model that displays the full range of ADHD associated behavioral phenotypes including working memory deficit, attention deficit and impulsive-like behavior. All of the ADHD-associated phenotypes respond to a single administration of a therapeutic equivalent dose of methylphenidate. In an earlier study, we showed that PNE produces hyperactivity, frontal cortical hypodopaminergic state and thinning of the cingulate cortex. Collectively, these data suggest that the PNE mouse model recapitulates key features of ADHD and may be a suitable preclinical model for ADHD research., (Copyright © 2017 ISDN. Published by Elsevier Ltd. All rights reserved.)
- Published
- 2017
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11. Motor System Activation Predicts Goal Imitation in 7-Month-Old Infants.
- Author
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Filippi CA, Cannon EN, Fox NA, Thorpe SG, Ferrari PF, and Woodward AL
- Subjects
- Brain Mapping methods, Cognition physiology, Electroencephalography methods, Female, Humans, Infant, Male, Mirror Neurons physiology, Social Behavior, Goals, Imitative Behavior physiology, Infant Behavior physiology, Motor Skills physiology, Psychomotor Performance physiology
- Abstract
The current study harnessed the variability in infants' neural and behavioral responses as a novel method for evaluating the potential relations between motor system activation and social behavior. We used electroencephalography (EEG) to record neural activity as 7-month-old infants observed and responded to the actions of an experimenter. To determine whether motor system activation predicted subsequent imitation behavior, we assessed event-related desynchronization (ERD) at central sites during action observation as a function of subsequent behavior. Greater mu desynchronization over central sites was observed when infants subsequently reproduced the experimenter's goal than when they did not reproduce the goal and instead selected the nongoal object. We also found that mu desynchronization during action execution predicted the infants' later propensity to reproduce the experimenter's goal-directed behavior. These results provide the first evidence that motor system activation predicts the imitation of other individuals' goals during infancy., (© The Author(s) 2016.)
- Published
- 2016
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12. Desynchronization in EEG during perception of means-end actions and relations with infants' grasping skill.
- Author
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Yoo KH, Cannon EN, Thorpe SG, and Fox NA
- Subjects
- Electroencephalography, Evoked Potentials, Female, Humans, Infant, Male, Motor Activity, Child Development physiology, Electroencephalography Phase Synchronization physiology, Hand Strength physiology, Infant Behavior physiology, Motor Skills physiology, Tool Use Behavior, Visual Perception physiology
- Abstract
The current study examined age-related differences in electroencephalogram (EEG) activity during perception of means-end actions and production of grasps, and how EEG activity may relate to infants' motor competence. We collected data from 9- and 12-month-old infants during perception of means-end actions made with a tool and during execution of their own grasps. We computed event-related desynchronization (ERD) during perception and production events and assessed infants' reach-grasp competence by looking at their latency to complete grasps. Although we found greater ERD during perception of means-end actions in 9-month-olds compared with 12-month-olds, we found the relation between ERD during perception and emerging reach-grasp competence to be specific for 12-month-olds and not for 9-month-olds. These results provide evidence for an emerging neural system that supports the coupling of action and perception with infants' emerging motor competence in the first year of life., (© 2015 The British Psychological Society.)
- Published
- 2016
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13. Assessing human mirror activity with EEG mu rhythm: A meta-analysis.
- Author
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Fox NA, Bakermans-Kranenburg MJ, Yoo KH, Bowman LC, Cannon EN, Vanderwert RE, Ferrari PF, and van IJzendoorn MH
- Subjects
- Humans, Brain Waves physiology, Mirror Neurons physiology, Motor Activity physiology, Visual Perception physiology
- Abstract
A fundamental issue in cognitive neuroscience is how the brain encodes others' actions and intentions. In recent years, a potential advance in our knowledge on this issue is the discovery of mirror neurons in the motor cortex of the nonhuman primate. These neurons fire to both execution and observation of specific types of actions. Researchers use this evidence to fuel investigations of a human mirror system, suggesting a common neural code for perceptual and motor processes. Among the methods used for inferring mirror system activity in humans are changes in a particular frequency band in the electroencephalogram (EEG) called the mu rhythm. Mu frequency appears to decrease in amplitude (reflecting cortical activity) during both action execution and action observation. The current meta-analysis reviewed 85 studies (1,707 participants) of mu that infer human mirror system activity. Results demonstrated significant effect sizes for mu during execution (Cohen's d = 0.46, N = 701) as well as observation of action (Cohen's d = 0.31, N = 1,508), confirming a mirroring property in the EEG. A number of moderators were examined to determine the specificity of these effects. We frame these meta-analytic findings within the current discussion about the development and functions of a human mirror system, and conclude that changes in EEG mu activity provide a valid means for the study of human neural mirroring. Suggestions for improving the experimental and methodological approaches in using mu to study the human mirror system are offered., ((c) 2016 APA, all rights reserved).)
- Published
- 2016
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14. Reversal Learning Deficits Associated with Increased Frontal Cortical Brain-Derived Neurotrophic Factor Tyrosine Kinase B Signaling in a Prenatal Cocaine Exposure Mouse Model.
- Author
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McCarthy DM, Bell GA, Cannon EN, Mueller KA, Huizenga MN, Sadri-Vakili G, Fadool DA, and Bhide PG
- Subjects
- Animals, Conditioning, Classical drug effects, Disease Models, Animal, Female, Mice, Pregnancy, Protein-Tyrosine Kinases metabolism, Receptor, trkB metabolism, Brain-Derived Neurotrophic Factor metabolism, Cocaine pharmacology, Frontal Lobe drug effects, Memory drug effects, Prenatal Exposure Delayed Effects physiopathology, Reversal Learning drug effects, Signal Transduction drug effects
- Abstract
Prenatal cocaine exposure remains a major public health concern because of its adverse impact on cognitive function in children and adults. We report that prenatal cocaine exposure produces significant deficits in reversal learning, a key component of cognitive flexibility, in a mouse model. We used an olfactory reversal learning paradigm and found that the prenatally cocaine-exposed mice showed a marked failure to learn the reversed paradigm. Because brain-derived neurotrophic factor (BDNF) is a key regulator of cognitive functions, and because prenatal cocaine exposure increases the expression of BDNF and the phosphorylated form of its receptor, tyrosine kinase B (TrkB), we examined whether BDNF-TrkB signaling is involved in mediating the reversal learning deficit in prenatally cocaine-exposed mice. Systemic administration of a selective TrkB receptor antagonist restored normal reversal learning in prenatally cocaine-exposed mice, suggesting that increased BDNF-TrkB signaling may be an underlying mechanism of reversal learning deficits. Our findings provide novel mechanistic insights into the reversal learning phenomenon and may have significant translational implications because impaired cognitive flexibility is a key symptom in psychiatric conditions of developmental onset., (© 2016 S. Karger AG, Basel.)
- Published
- 2016
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15. Spectral and source structural development of mu and alpha rhythms from infancy through adulthood.
- Author
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Thorpe SG, Cannon EN, and Fox NA
- Subjects
- Adolescent, Age Factors, Child, Preschool, Electroencephalography methods, Female, Humans, Infant, Male, Movement physiology, Photic Stimulation methods, Young Adult, Alpha Rhythm physiology, Motor Cortex growth & development, Psychomotor Performance physiology
- Abstract
Objective: To assess the developmental trajectory of spectral, topographic, and source structural properties of functional mu desynchronization (characterized during voluntary reaching/grasping movement), and investigate its spectral/topographic relation to spontaneous EEG in the developing alpha band., Methods: Event related desynchronization (ERD) and power spectral density spectra/topography are analyzed in 12 month-old infants, 4 year-old children, and adults. Age-matched head models derived from structural MRI are used to obtain current density reconstructions of mu desynchronization across the cortical surface., Results: Infant/child EEG contains spectral peaks evident in both the upper and lower developing alpha band, and spectral/topographic properties of functionally identified mu rhythm strongly reflect those of upper alpha in all subject groups. Source reconstructions show distributed frontoparietal patterns of cortical mu desynchronization concentrated in specific central and parietal regions which are consistent across age groups., Conclusions: Peak frequencies of mu desynchronization and spontaneous alpha band EEG increase with age, and characteristic mu topography/source-structure is evident in development at least as early as 12 months., Significance: Results provide evidence for a cortically distributed functional mu network, with spontaneous activity measurable in the upper alpha band throughout development., (Copyright © 2015 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.)
- Published
- 2016
- Full Text
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16. Relations between infants' emerging reach-grasp competence and event-related desynchronization in EEG.
- Author
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Cannon EN, Simpson EA, Fox NA, Vanderwert RE, Woodward AL, and Ferrari PF
- Subjects
- Adult, Behavior physiology, Brain physiology, Female, Humans, Infant, Intention, Male, Observation, Brain Mapping methods, Electroencephalography methods, Motor Skills physiology, Perception physiology, Psychomotor Performance physiology
- Abstract
Recent reports of similar patterns of brain electrical activity (electroencephalogram: EEG) during action execution and observation, recorded from scalp locations over motor-related regions in infants and adults, have raised the possibility that two foundational abilities--controlling one's own intentional actions and perceiving others' actions--may be integrally related during ontogeny. However, to our knowledge, there are no published reports of the relations between developments in motor skill (i.e. recording actual motor skill performance) and EEG during both action execution and action observation. In the present study we collected EEG from 21 9-month-olds who were given opportunities to reach for toys and who also observed an experimenter reach for toys. Event-related desynchronization (ERD) was computed from the EEG during the reaching events. We assessed infants' reaching-grasping competence, including reach latency, errors, preshaping of the hand, and bimanual reaches, and found that desynchronization recorded in scalp electrodes over motor-related regions during action observation was associated with action competence during execution. Infants who were more competent reachers, compared to less competent reachers, exhibited greater ERD while observing reaching-grasping. These results provide initial evidence for an early emerging neural system integrating one's own actions with the perception of others' actions., (© 2015 John Wiley & Sons Ltd.)
- Published
- 2016
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17. Prenatal Cocaine Exposure Alters BDNF-TrkB Signaling in the Embryonic and Adult Brain.
- Author
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McCarthy DM, Mueller KA, Cannon EN, Huizenga MN, Darnell SB, Bhide PG, and Sadri-Vakili G
- Subjects
- Aging, Animals, Brain growth & development, Female, Mice, Pregnancy, Prosencephalon metabolism, Protein-Tyrosine Kinases metabolism, RNA, Messenger metabolism, Receptor, trkB genetics, Brain drug effects, Brain-Derived Neurotrophic Factor metabolism, Cocaine pharmacology, Prenatal Exposure Delayed Effects metabolism, Receptor, trkB metabolism, Signal Transduction drug effects
- Abstract
Prenatal cocaine exposure remains a major public health concern because of its adverse effects on cognitive function. Although the molecular mechanisms underlying the cognitive impairment are not fully understood, brain-derived neurotrophic factor (BDNF) signaling via its receptor tyrosine kinase B (TrkB) is emerging as a potential candidate. We used a mouse model to examine the impact of ongoing cocaine exposure on BDNF expression in the dorsal forebrain on embryonic day 15 (E15) as well as the long-term effects of prenatal cocaine exposure on BDNF-TrkB signaling in the frontal cortex in early postnatal (postnatal day 16; P16) and adult (P60) male and female mice. We found that ongoing cocaine exposure decreased BDNF expression in the E15 dorsal forebrain, prenatal cocaine exposure did not alter BDNF or TrkB (total or phosphorylated) expression in the frontal cortex at P16, and that the prenatal cocaine exposure produced significant increases in BDNF, the activated (phosphorylated) form of TrkB, as well as Bdnf mRNA in the frontal cortex at P60. The increase in BDNF protein and mRNA expression at P60 was concurrent with hyperacetylation of histone H3 at the Bdnf promoter in the frontal cortex. The increase in frontal cortical BDNF and activated TrkB at P60 occurred in male but not female mice. Thus, our data demonstrate that ongoing cocaine exposure produces a decrease in BDNF expression in the embryonic brain, and that prenatal cocaine exposure produces a sex-specific increase in frontal cortical BDNF-TrkB signaling at P60 only in male mice. Lastly, hyperacetylation of histone H3 at the Bdnf promoter is one epigenetic mechanism mediating the effects of prenatal cocaine exposure on Bdnf expression at P60 in male mice., (© 2017 S. Karger AG, Basel.)
- Published
- 2016
- Full Text
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18. Hypervigilance to Rejecting Stimuli in Rejection Sensitive Individuals: Behavioral and Neurocognitive Evidence.
- Author
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Ehrlich KB, Gerson SA, Vanderwert RE, Cannon EN, and Fox NA
- Abstract
Individuals who are high in rejection sensitivity are vigilant toward social cues that signal rejection, and they exhibit attention biases towards information that confirms expectations of rejection. Little is known, however, about the neural correlates of rejection sensitivity. The present study examined whether rejection sensitivity is associated with individuals' neural responses to rejection-relevant information. Female participants, classified as high or average in rejection sensitivity, completed a modified dot-probe task in which a neutral face was paired with either another neutral face or a gaze-averted ("rejecting") face while EEG was collected and ERP components were computed. Behavioral results indicated that average rejection sensitive participants showed an attention bias away from rejecting faces, while high rejection sensitive participants were equally vigilant to neutral and rejecting faces. High rejection sensitivity was associated with ERP components signaling elevated attention and arousal to faces. These findings suggest that rejection sensitivity shapes behavioral and neurocognitive responses to faces.
- Published
- 2015
- Full Text
- View/download PDF
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