scholarly journals Distinct Processing of Selection and Execution Errors in Neural Signatures of Outcome Monitoring

2019 ◽  
Author(s):  
Faisal Mushtaq ◽  
Samuel D. McDougle ◽  
Matt P. Craddock ◽  
Darius E. Parvin ◽  
Jack Brookes ◽  
...  
Keyword(s):  
Behavioral Adjustment ◽  
Behavioral Changes ◽  
Behavioral Correlates ◽  
Feedback Information ◽  
Future Action ◽  
Outcome Monitoring ◽  
Frontal Negativity ◽  
Neural Signature ◽  
The Brain ◽  
Insight Into

AbstractLosing a point playing tennis may result from poor shot selection or poor stroke execution. To explore how the brain responds to these different types of errors, we examined EEG signatures of feedback-related processing while participants performed a simple decision-making task. In Experiment 1, we used a task in which unrewarded outcomes were framed as selection errors, similar to how feedback information is treated in most studies. Consistent with previous work, EEG differences between rewarded and unrewarded trials in the medial frontal negativity (MFN) correlated with behavioral adjustment. In Experiment 2, the task was modified such that unrewarded outcomes could arise from either poor execution or selection. For selection errors, the results replicated that observed in Experiment 1. However, unrewarded outcomes attributed to poor execution produced larger amplitude MFN, alongside an attenuation in activity preceding this component and a subsequent enhanced error positivity (Pe) response in posterior sites. In terms of behavioral correlates, only the degree of the early attenuation and amplitude of the Pe correlated with behavioral adjustment following execution errors relative to reward; the amplitude of the MFN did not correlate with behavioral changes related to execution errors. These results indicate the existence of distinct neural correlates of selection and execution error processing and are consistent with the hypothesis that execution errors can modulate action selection evaluation. More generally, they provide insight into how the brain responds to different classes of error that determine future action.Significance StatementTo learn from mistakes, we must resolve whether decisions that fail to produce rewards are due to poorly selected action plans or badly executed movements. EEG data were obtained to identify and compare the physiological correlates of selection and execution errors, and how these are related to behavioral changes. A neural signature associated with reinforcement learning, a medial frontal negative (MFN) ERP deflection, correlated with behavioral adjustment after selection errors relative to reward outcomes, but not motor execution errors. In contrast, activity preceding and following the MFN response correlated with behavioral adjustment after execution errors relative to reward. These results provide novel insight into how the brain responds to different classes of error that determine future action.

scholarly journals Decreased Taurine and Creatine in the Thalamus May Relate to Behavioral Impairments in Ethanol-Fed Mice: A Pilot Study of Proton Magnetic Resonance Spectroscopy

2018 ◽  
Vol 17 ◽  
pp. 153601211774905 ◽  
Author(s):  
Su Xu ◽  
Wenjun Zhu ◽  
Yamin Wan ◽  
JiaBei Wang ◽  
Xi Chen ◽  
...  
Keyword(s):  
Hepatic Encephalopathy ◽  
Magnetic Resonance ◽  
Magnetic Resonance Spectroscopy ◽  
Proton Magnetic Resonance ◽  
Proton Magnetic Resonance Spectroscopy ◽  
Minimal Hepatic Encephalopathy ◽  
Behavioral Changes ◽  
Resonance Spectroscopy ◽  
The Brain ◽  
Insight Into

Minimal hepatic encephalopathy (MHE) is highly prevalent, observed in up to 80% of patients with liver dysfunction. Minimal hepatic encephalopathy is defined as hepatic encephalopathy with cognitive deficits and no grossly evident neurologic abnormalities. Clinical management may be delayed due to the lack of in vivo quantitative methods needed to reveal changes in brain neurobiochemical biomarkers. To gain insight into the development of alcoholic liver disease–induced neurological dysfunction (NDF), a mouse model of late-stage alcoholic liver fibrosis (LALF) was used to investigate changes in neurochemical levels in the thalamus and hippocampus that relate to behavioral changes. Proton magnetic resonance spectroscopy of the brain and behavioral testing were performed to determine neurochemical alterations and their relationships to behavioral changes in LALF. Glutamine levels were higher in both the thalamus and hippocampus of alcohol-treated mice than in controls. Thalamic levels of taurine and creatine were significantly diminished and strongly correlated with alcohol-induced behavioral changes. Chronic long-term alcohol consumption gives rise to advanced liver fibrosis, neurochemical changes in the nuclei, and behavioral changes which may be linked to NDF. Magnetic resonance spectroscopy represents a sensitive and noninvasive measurement of pathological alterations in the brain, which may provide insight into the pathogenesis underlying the development of MHE.

scholarly journals Opposing roles of primate areas 25 and 32 and their putative rodent homologs in the regulation of negative emotion

2017 ◽  
Vol 114 (20) ◽  
pp. E4075-E4084 ◽  
Author(s):  
Chloe U. Wallis ◽  
Rudolf N. Cardinal ◽  
Laith Alexander ◽  
Angela C. Roberts ◽  
Hannah F. Clarke
Keyword(s):  
Negative Emotion ◽  
Brain Regions ◽  
Emotional Dysregulation ◽  
Anxiety And Depression ◽  
Depression And Anxiety ◽  
Behavioral Correlates ◽  
The Brain ◽  
Insight Into ◽  
Human Neuroimaging

Disorders of dysregulated negative emotion such as depression and anxiety also feature increased cardiovascular mortality and decreased heart-rate variability (HRV). These disorders are correlated with dysfunction within areas 25 and 32 of the ventromedial prefrontal cortex (vmPFC), but a causal relationship between dysregulation of these areas and such symptoms has not been demonstrated. Furthermore, cross-species translation is limited by inconsistent findings between rodent fear extinction and human neuroimaging studies of negative emotion. To reconcile these literatures, we applied an investigative approach to the brain–body interactions at the core of negative emotional dysregulation. We show that, in marmoset monkeys (a nonhuman primate that has far greater vmPFC homology to humans than rodents), areas 25 and 32 have causal yet opposing roles in regulating the cardiovascular and behavioral correlates of negative emotion. In novel Pavlovian fear conditioning and extinction paradigms, pharmacological inactivation of area 25 decreased the autonomic and behavioral correlates of negative emotion expectation, whereas inactivation of area 32 increased them via generalization. Area 25 inactivation also increased resting HRV. These findings are inconsistent with current theories of rodent/primate prefrontal functional similarity, and provide insight into the role of these brain regions in affective disorders. They demonstrate that area 32 hypoactivity causes behavioral generalization relevant to anxiety, and that area 25 is a causal node governing the emotional and cardiovascular symptomatology relevant to anxiety and depression.

scholarly journals Addiction as a brain disease revised: why it still matters, and the need for consilience

2021 ◽  
Author(s):  
Markus Heilig ◽  
James MacKillop ◽  
Diana Martinez ◽  
Jürgen Rehm ◽  
Lorenzo Leggio ◽  
...  
Keyword(s):  
Spontaneous Remission ◽  
Brain Disease ◽  
Substance Addiction ◽  
Alternative Reinforcement ◽  
Sociocultural Perspectives ◽  
Compulsive Behaviors ◽  
Biological Substrate ◽  
Neural Signature ◽  
The Brain ◽  
Neuroscience Community

AbstractThe view that substance addiction is a brain disease, although widely accepted in the neuroscience community, has become subject to acerbic criticism in recent years. These criticisms state that the brain disease view is deterministic, fails to account for heterogeneity in remission and recovery, places too much emphasis on a compulsive dimension of addiction, and that a specific neural signature of addiction has not been identified. We acknowledge that some of these criticisms have merit, but assert that the foundational premise that addiction has a neurobiological basis is fundamentally sound. We also emphasize that denying that addiction is a brain disease is a harmful standpoint since it contributes to reducing access to healthcare and treatment, the consequences of which are catastrophic. Here, we therefore address these criticisms, and in doing so provide a contemporary update of the brain disease view of addiction. We provide arguments to support this view, discuss why apparently spontaneous remission does not negate it, and how seemingly compulsive behaviors can co-exist with the sensitivity to alternative reinforcement in addiction. Most importantly, we argue that the brain is the biological substrate from which both addiction and the capacity for behavior change arise, arguing for an intensified neuroscientific study of recovery. More broadly, we propose that these disagreements reveal the need for multidisciplinary research that integrates neuroscientific, behavioral, clinical, and sociocultural perspectives.

Effects of the SNAP25 on Integration Ability of Brain Functions in Children With ADHD

2020 ◽  
pp. 108705472096456
Author(s):  
Yue Yang ◽  
Gang Peng ◽  
Hongwu Zeng ◽  
Diangang Fang ◽  
Linlin Zhang ◽  
...  
Keyword(s):  
Time Window ◽  
Precentral Gyrus ◽  
Children With Adhd ◽  
Brain Functions ◽  
Lingual Gyrus ◽  
Window Method ◽  
Central Gyrus ◽  
The Right ◽  
The Brain ◽  
Insight Into

Objective: The present study aimed to examine the effects of SNAP25 on the integration ability of intrinsic brain functions in children with ADHD, and whether the integration ability was associated with working memory (WM). Methods: A sliding time window method was used to calculate the spatial and temporal concordance among five rs-fMRI regional indices in 55 children with ADHD and 20 healthy controls. Results: The SNAP25 exhibited significant interaction effects with ADHD diagnosis on the voxel-wise concordance in the right posterior central gyrus, fusiform gyrus and lingual gyrus. Specifically, for children with ADHD, G-carriers showed increased voxel-wise concordance in comparison to TT homozygotes in the right precentral gyrus, superior frontal gyrus, postcentral gyrus, and middle frontal gyrus. The voxel-wise concordance was also found to be related to WM. Conclusion: Our findings provided a new insight into the neural mechanisms of the brain function of ADHD children.

scholarly journals Pain Detection and the Privacy of Subjective Experience

2007 ◽  
Vol 33 (2-3) ◽  
pp. 433-456 ◽  
Author(s):  
Adam J. Kolber
Keyword(s):  
Subjective Experience ◽  
Brain Regions ◽  
Physical Pain ◽  
Medical Evidence ◽  
Functional Magnetic Resonance ◽  
Positron Emission ◽  
Pain Symptoms ◽  
The Brain ◽  
Insight Into ◽  
Neuroimaging Techniques

A neurologist with abdominal pain goes to see a gastroenterologist for treatment. The gastroenterologist asks the neurologist where it hurts. The neurologist replies, “In my head, of course.” Indeed, while we can feel pain throughout much of our bodies, pain signals undergo most of their processing in the brain. Using neuroimaging techniques like functional magnetic resonance imaging (“fMRI”) and positron emission tomography (“PET”), researchers have more precisely identified brain regions that enable us to experience physical pain. Certain regions of the brain's cortex, for example, increase in activation when subjects are exposed to painful stimuli. Furthermore, the amount of activation increases with the intensity of the painful stimulus. These findings suggest that we may be able to gain insight into the amount of pain a particular person is experiencing by non-invasively imaging his brain.Such insight could be particularly valuable in the courtroom where we often have no definitive medical evidence to prove or disprove claims about the existence and extent of pain symptoms.

scholarly journals Modafinil Effects on Behavior and Oxidative Damage Parameters in Brain of Wistar Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Felipe Ornell ◽  
Samira S. Valvassori ◽  
Amanda V. Steckert ◽  
Pedro F. Deroza ◽  
Wilson R. Resende ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Open Field ◽  
Wistar Rats ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
Behavioral Changes ◽  
Protein Damage ◽  
Behavioral Parameters ◽  
Carbonyl Formation ◽  
The Brain

The effects of modafinil (MD) on behavioral and oxidative damage to protein and lipid in the brain of rats were evaluated. Wistar rats were given a single administration by gavage of water or MD (75, 150, or 300 mg/kg). Behavioral parameters were evaluated in open-field apparatus 1, 2, and 3 h after drug administration. Thiobarbituric acid reactive substances (TBARS) and protein carbonyl formation were measured in the brain. MD increased locomotor activity at the highest dose 1 and 3 h after administration. MD administration at the dose of 300 mg/kg increased visits to the center of open-field 1 h after administration; however, 3 h after administration, all administered doses of MD increased visits to the open-field center. MD 300 mg/kg increased lipid damage in the amygdala, hippocampus, and striatum. Besides, MD increased protein damage in the prefrontal cortex, amygdala, and hippocampus; however, this effect varies depending on the dose administered. In contrast, the administration of MD 75 and 300 mg/kg decreased the protein damage in the striatum. This study demonstrated that the MD administration induces behavioral changes, which was depending on the dose used. In addition, the effects of MD on oxidative damage parameters seemed to be in specific brain region and doses.

scholarly journals Distinct Roles of Deiodinases on the Phenotype of Mct8 Defect: A Comparison of Eight Different Mouse Genotypes

Endocrinology ◽  
2011 ◽  
Vol 152 (3) ◽  
pp. 1180-1191 ◽  
Author(s):  
Xiao-Hui Liao ◽  
Caterina Di Cosmo ◽  
Alexandra M. Dumitrescu ◽  
Arturo Hernandez ◽  
Jacqueline Van Sande ◽  
...  
Keyword(s):  
Growth Response ◽  
Pituitary Thyroid Axis ◽  
Severe Impairment ◽  
Serum T3 ◽  
Serum T4 ◽  
Thyroid Axis ◽  
Mct8 Deficiency ◽  
The Brain ◽  
Insight Into ◽  
Serum Tsh

Mice deficient in the thyroid hormone (TH) transporter Mct8 (Mct8KO) have increased 5′-deiodination and impaired TH secretion and excretion. These and other unknown mechanisms result in the low-serum T4, high T3, and low rT3 levels characteristic of Mct8 defects. We investigated to what extent each of the 5′-deiodinases (D1, D2) contributes to the serum TH abnormalities of the Mct8KO by generating mice with all combinations of Mct8 and D1 and/or D2 deficiencies and comparing the resulting eight genotypes. Adding D1 deficiency to that of Mct8 corrected the serum TH abnormalities of Mct8KO mice, normalized brain T3 content, and reduced the impaired expression of TH-responsive genes. In contrast, Mct8D2KO mice maintained the serum TH abnormalities of Mct8KO mice. However, the serum TSH level increased 27-fold, suggesting a severely impaired hypothalamo-pituitary-thyroid axis. The brain of Mct8D2KO manifested a pattern of more severe impairment of TH action than Mct8KO alone. In triple Mct8D1D2KO mice, the markedly increased serum TH levels produced milder brain defect than that of Mct8D2KO at the expense of more severe liver thyrotoxicosis. Additionally, we observed that mice deficient in D2 had an unexplained marked reduction in the thyroid growth response to TSH. Our studies on these eight genotypes provide a unique insight into the complex interplay of the deiodinases in the Mct8 defect and suggest that D1 contributes to the increased serum T3 in Mct8 deficiency, whereas D2 mainly functions locally, converting T4 to T3 to compensate for distinct cellular TH depletion in Mct8KO mice.

scholarly journals Diving into the world of alcohol teratogenesis: a review of zebrafish models of fetal alcohol spectrum disorder

2018 ◽  
Vol 96 (2) ◽  
pp. 88-97 ◽  
Author(s):  
Yohaan Fernandes ◽  
Desire M. Buckley ◽  
Johann K. Eberhart
Keyword(s):  
Fetal Alcohol Spectrum Disorder ◽  
Model Organism ◽  
Spectrum Disorder ◽  
Structural Defects ◽  
Craniofacial Skeleton ◽  
Fetal Alcohol ◽  
Embryonic Exposure ◽  
Fetal Alcohol Spectrum ◽  
The Brain ◽  
Insight Into

The term fetal alcohol spectrum disorder (FASD) refers to the entire suite of deleterious outcomes resulting from embryonic exposure to alcohol. Along with other reviews in this special issue, we provide insight into how animal models, specifically the zebrafish, have informed our understanding of FASD. We first provide a brief introduction to FASD. We discuss the zebrafish as a model organism and its strengths for alcohol research. We detail how zebrafish has been used to model some of the major defects present in FASD. These include behavioral defects, such as social behavior as well as learning and memory, and structural defects, disrupting organs such as the brain, sensory organs, heart, and craniofacial skeleton. We provide insights into how zebrafish research has aided in our understanding of the mechanisms of ethanol teratogenesis. We end by providing some relatively recent advances that zebrafish has provided in characterizing gene-ethanol interactions that may underlie FASD.

scholarly journals Contribution of Neuroinflammation to the Pathogenesis of Cancer Cachexia

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Alessio Molfino ◽  
Gianfranco Gioia ◽  
Filippo Rossi Fanelli ◽  
Alessandro Laviano
Keyword(s):  
Adipose Tissue ◽  
Food Intake ◽  
Proinflammatory Cytokines ◽  
Adaptive Response ◽  
Energy Homeostasis ◽  
Cancer Cachexia ◽  
Behavioral Changes ◽  
Brain Areas ◽  
Functional Changes ◽  
The Brain

Inflammation characterizes the course of acute and chronic diseases and is largely responsible for the metabolic and behavioral changes occurring during the clinical journey of patients. Robust data indicate that, during cancer, functional modifications within brain areas regulating energy homeostasis contribute to the onset of anorexia, reduced food intake, and increased catabolism of muscle mass and adipose tissue. In particular, functional changes are associated with increased hypothalamic concentration of proinflammatory cytokines, which suggests that neuroinflammation may represent the adaptive response of the brain to peripheral challenges, including tumor growth. Within this conceptual framework, the vagus nerve appears to be involved in conveying alert signals to the hypothalamus, whereas hypothalamic serotonin appears to contribute to triggering catabolic signals.

scholarly journals Reflections on the Constraints and Opportunities in Therapy in Rett Syndrome

2006 ◽  
Vol 6 ◽  
pp. 992-997 ◽  
Author(s):  
Alison M. Kerr
Keyword(s):  
Quality Of Life ◽  
Neural Networks ◽  
Rett Syndrome ◽  
Clear Understanding ◽  
Research Experience ◽  
Hormonal Responses ◽  
Physical Limitations ◽  
The Brain ◽  
Insight Into

More than 20 years of clinical and research experience with affected people in the British Isles has provided insight into particular challenges for therapists, educators, or parents wishing to facilitate learning and to support the development of skills in people with Rett syndrome. This paper considers the challenges in two groups: those due to constraints imposed by the disabilities associated with the disorder and those stemming from the opportunities, often masked by the disorder, allowing the development of skills that depend on less-affected areas of the brain. Because the disorder interferes with the synaptic links between neurones, the functions of the brain that are most dependent on complex neural networks are the most profoundly affected. These functions include speech, memory, learning, generation of ideas, and the planning of fine movements, especially those of the hands. In contrast, spontaneous emotional and hormonal responses appear relatively intact. Whereas failure to appreciate the physical limitations of the disease leads to frustration for therapist and client alike, a clear understanding of the better-preserved areas of competence offers avenues for real progress in learning, the building of satisfying relationships, and achievement of a quality of life.

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