Guide Altered Circuits

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I can read theory, but having someone simply explain "this part does this" shows me "why" a circuit is built the way it is I love this stuff because it CAN be made understandable if the right examples are given. How is frequency modulated in this circuit? What exactly is every element in that part doing? Posted by 2Izzy in forum: Find frequency in a circuit without Xc Posted by 7Axis in forum: How is a frequency response curve made?

Posted by meyerb in forum: Sinusoidal Variable Frequency Oscillator in a small Circuit? Is there a simple way? Posted by thatsoutherly in forum: What is the frequency range of a signal generator in circuit maker? You May Also Like: Here's a quick look at some recent haptic technology-related news. Simplify Your Lighting Design: Negative Feedback, Part 6: New and Improved Stability Analysis This article will show you a handy alternative approach to assessing stability via open-loop gain and the feedback factor.

Altered Brain Reward Circuits in Eating Disorders: Chicken or Egg?

Your name or email address: These findings are surprising and very important because they contradict the common thinking that the brain circuits damaged during the childhood cannot improve in the adulthood. The new genetic strategies promise to be a powerful tool looking at the possibility of future treatments for disorders like RTT and ASD.

However, a necessary intermediate step will be the use of transgenic animals closer to our species, such as primates, to test the reliability of such technologies and their safety for our health. Anyway, the genetic manipulation of specific circuits of the brain and the first good results obtained in animal models give us the concrete hope to develop effective methods to help RTT and autistic patient in the future. Post navigation The big challenge of the brain circuits STXBP1 protein as a therapeutic target for Epileptic Encephalopathy Connecting the growing brain network of specialised clinicians and researchers.

People and labs around the world with the aim to understand the developing brain through synaptic communication. The challenge of our project is to build bridges between different disciplines that are normally practiced one far apart from the other. Lorem ipsum dolor sit amet, consectetur adipiscing elit. Further, computational models exist that allow making inferences regarding brain dopamine activation based on type and frequency of food stimulus exposure. Such a model is the temporal difference model [ 38 ], a computational theoretical framework for reward learning that is based on brain dopamine activation response to receiving of expected or unexpected reward stimuli.

The primary areas that have been associated with that model are the ventral tegmental area and anteroventral striatum. In short, when we subject an individual to conditions of receipt or omission of expected or unexpected food stimuli, we can study brain dopamine associated reward pathways using brain imaging. This model has been studied in dopamine neurons and adapted to human brain imaging [ 39 ].

Differences in brain response across ED and healthy individuals using this model then could provide us with information about possible dopamine related brain function and changes in EDs. Research in AN indicated dopamine alterations such as altered levels of dopamine metabolites in the brain or number of dopamine receptors in specific brain regions [ 40 — 43 ], but we know little how such alterations may be clinically important. Functional brain imaging may help bridge this gap. Recovered AN showed reduced brain response to repeated sweet taste in insula and striatum [ 45 ], but increased caudate response to randomly given monetary [ 46 ] or taste stimuli [ 47 ].

The discrepancy in response between repeated versus randomly applied taste stimuli across studies is most likely due to the random application stimulating the unconditioned dopamine related prediction error response while during the repeated application we expect that cognitive factors play a bigger role and affect reward response. For instance individuals with AN who know about a taste stimulus approaching as in the repeated application of a taste may constrain themselves in order to avoid an unwanted or as excessive perceived reward system response out of fear of overstimulation and food avoidance [ 49 ].

BN has been associated with addiction disorders [ 50 ] due to the episodic and often compulsive binging on palatable foods. The same neural pathways that reinforce motivation to approach food are also activated in response to addictive drugs [ 51 ].

Braincell - Attack of the Circuits

In summary, prediction error brain response is on opposite ends between AN and BN groups and promises to be an excellent construct to model brain reward function in EDs that could be related to dopamine function. This construct could also be useful in capturing state dependent and maybe also trait related brain response on trajectories of types or severity of ED related behavior.


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Two other recent studies suggest possible state versus trait related brain alterations in EDs. First, a study in recovered AN and BN individuals that applied repeated caloric and non-caloric sweet taste stimuli during fMRI showed in recovered AN individuals reduced but in recovered BN subjects increased insula response compared to controls [ 55 ]. With the notion in mind that alterations after recovery could indicate premorbid or trait alterations in those individuals, those results implicate the insula as maybe important in the development of EDs. However, as it is a functional study, the altered response could be directly due to insula function, or could be due to altered input from other brain regions affecting insula activity.

A recent structural study from our group showed that in ill and recovered AN as well as ill BN individuals orbitofrontal cortex gyrus rectus volume was higher compared to controls, suggesting that this could be a trait alteration across EDs [ 56 ]. That study further found that ill and recovered AN had higher right, while BN individuals had higher left insula volume.

The fixed perception of being fat while severely underweight in anorexia nervosa [ 59 ] could thus be due to a right dysfunctional insula. The left insula activation responds to gastric distention [ 60 ] and self-reported fullness [ 61 ]. Importantly, those results of higher insula volume [ 56 ] are discrepant from most other studies on brain structure in AN that had found lower brain volumes compared to controls [ 62 ].

We believe this is due to the fact that subjects in our studies were assessed after 1—2 weeks of controlled food intake, which should have resolved effects from acute starvation and ideally identify regions that contribute to ED psychopathology. A caveat here is that all those studies will need replication in larger samples and whether the left and right distinctions will hold remains to be seen. Clinically, individuals with EDs stand out to be anxious and cautious, and research has suggested both anxious traits such as harm avoidance as well as increased prevalence of premorbid anxiety disorders [ 63 , 64 ].

Thus, anxiety has been suggested to be a key vulnerability factor for the development of EDs [ 65 ]. In addition, AN and BN have been found to have emotion regulation difficulties [ 66 , 67 ], and ED individuals appear to control their eating, weight and shape as a way to address their perceived lack of control over interpersonal and overall life stressors and overwhelming anxiety [ 64 , 68 ]. This need for control could be driven by highly elevated scores of intolerance of uncertainty in both AN and BN [ 69 ].

In summary, with the high anxious behaviors observed in EDs, fear related brain pathways should be involved in those disorders. Food and related weight gain are still the primary fear inducing stimuli for ED individuals. Various studies have applied pictures of high and low calorie foods during brain imaging to elicit brain response in relation to anxiety ratings. In AN for instance high-calorie food pictures provoked anxiety and led to greater temporo-occipital activation and mesial temporal as well as left insular and bilateral anterior cingulate activity, and these results were thought to be consistent with anxiety provocation and related limbic activation [ 70 ].

In another study [ 71 ] food images stimulated medial prefrontal and anterior cingulate cortex in recovered and ill AN, but lateral prefrontal regions only in recovered AN. In recovered AN, prefrontal cortex, anterior cingulate cortex and cerebellum were more highly activated compared to both controls and chronic AN after food presentation. This suggested that higher anterior cingulate cortex and medial prefrontal cortex activity in both ill and recovered AN compared to controls may be a trait marker for AN.

These are areas of executive function, decision-making, error monitoring and also reward expectancy. Such alterations could suggest heightened vigilance or processing activity in response to visual food stimuli. Taken together, these studies suggest that the frontal cortex is active in the capacity to appropriately or inappropriately restrict food, possibly via heightened fear related activation and anxious cognitions that drive food restriction.

Introduction

Just recently, we applied diffusion tensor imaging DTI in AN, a technique that investigates integrity of white matter tracts in the brain [ 72 ]. That study indicated the there are white matter alterations in AN in particular in the bilateral fimbria fornix regions, outflux pathways from the hippocampus and connecting to frontal cortical regions and subcortical reward processing areas such as the ventral striatum, and importantly fimbria fornix white matter alterations in AN predicted harm avoidance.

This study thus suggests that alterations in white matter could be directly involved in the pathophysiology of anxiety processing in AN. In BN, presentation of food images was also associated with increased response in frontal, cingulate, occipital and insula cortex, and suggesting anxious response as in the AN group [ 71 ].

In summary, one could hypothesize the following model of a functional disconnect between brain regions. The AN individual is initially learning to overvalue extreme ideals of thinness, and the amygdala get sensitized to food and body related stimuli as threatening and starts to restrict food. With illness progression there is an increasing lack of connectivity between frontal cortex and amygdala, possibly related to altered white matter connectivity [ 72 ].

This may lead to an inability of prefrontal brain regions to control excessive amygdala activity, which continues to drive weight related fears, even if an AN individual tries to reverse course. This continuous fear response could be a reinforcing mechanism that further worsens known poor cognitive flexibility in AN [ 73 ] in reevaluating actual danger of shape and weight related stimuli, and an inability to test and adapt to new behaviors such as re-feeding and weight gain. Additionally, a pathologic integration of signals from the body periphery may disturb normal body image and drive the perception of being fat despite being thin.

Studying ED individuals premorbidly is difficult because of the low incidence of the disorder.

Studying individuals after recovery may be the closest to reflect brain function that may have been before start of the illness. Based on the above described studies we propose Table 1 that individuals with EDs have as trait abnormality larger orbitofrontal cortex volumes compared to controls, which may contribute to early satiety and disturbed valuation of food stimuli. ED subjects are generally anxious and this is reflected in high frontal and anterior cingulate cortex activation, which may also be a premorbid trait.

When environmental stress and low self valuation trigger fear of fatness, this hyperactive circuitry will be high jacked by those fears and provide the neurobiological correlate for preoccupation with body related fears and food concerns. Times of food restriction in AN then may sensitize insula and striatal reward pathways and contribute to overstimulation of an already hypersensitive salience response [ 49 ] and drive food avoidance from a biological level. Low response to repeated and thus predictable food stimuli may be due to higher order cognitive processes controlling the lower brain circuitry in order to avoid too strong salient stimulus stimulation.

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In BN, fear driven food restriction may collide with a possibly trait related hypo-responsive reward system that predisposes to binge eating, and that behavior then even more decreases reward sensitivity in response to excessive food intake. During acute food restriction or episodes of purging, brain volumes may decrease due to the lack of fluids [ 74 ], but higher orbitofrontal and insula cortex volumes may be present before, during and after recovery, when controlling for acute malnutrition.

It is possible that increased right insula volume predisposes especially restricting type AN individuals to have disturbed interoception and body experience [ 59 ] and while a possible trait of higher left sided insula volume in BN could prejudice those individuals to be more sensitive to gastrointestinal perception [ 60 , 61 ] and promote the need to alleviate fullness by self induced vomiting. The functional responses to reward increased in AN, decreased in BN and anxiety increased in AN and BN specific tasks will adapt during the course of illness of EDs and will be exaggerated compared to the premorbid state.

With ongoing illness, food restriction will further heighten sensitivity to salient stimuli in AN, while binge eating and purging behavior will more and more reduce reward responsiveness in BN.

HOW is Frequency Altered in a Circuit?

By the same time AN and BN individuals both struggle with shape and weight related fears, which drive the seemingly illogical presentation of rather continuing the ED illness behavior than work on recovery. This is because the fear and anxiety are just so intolerable for them and the particular illness behavior at least in the moment alleviates their fears more than normalization of eating behavior.

EDs are multifactorial illnesses with a variety of bio-psychosocial aspects, yet they run in families and there should be strong biological factors that predispose ED individuals to developing those disorders. In this synthesis of some of the most recent ED brain imaging literature I proposed a model of potential predisposing structural and functional brain alterations that could contribute to the development of EDs and why it may be so difficult to overcome them.