When food porn holds no allure: the science behind satiety

New research from the University of British Columbia is shedding light on why enticing pictures of food affect us less when we’re full.

“We’ve known that insulin plays a role in telling us we’re satiated after eating, but the mechanism by which this happens is unclear,” says Stephanie Borgland, an assistant professor in UBC’s Dept. of Anesthesiology, Pharmacology and Therapeutics and the study’s senior author.

In the new study published online this week in Nature Neuroscience, Borgland and colleagues found that insulin – prompted by a sweetened, high-fat meal – affects the ventral tegmental area (VTA) of the brain, which is responsible for reward-seeking behaviour. When insulin was applied to the VTA in mice, they no longer gravitated towards environments where food had been offered.

“Insulin dulls the synapses in this region of the brain and decreases our interest in seeking out food,” says Borgland, “which in turn causes us to pay less attention to food-related cues.”

“There has been a lot of discussion around the environmental factors of the obesity epidemic,” Borgland adds, pointing to fast food advertising bans in Quebec, Norway, the U.K., Greece and Sweden. “This study helps explain why pictures or other cues of food affect us less when we’re satiated – and may help inform strategies to reduce environmental triggers of overeating.”

The VTA has also been shown to be associated with addictive behaviours, including illicit drug use. Borgland says better understanding of the mechanism in this region of the brain could, in the long run, inform diagnosis and treatment.

(Image: Shutterstock)

Glial cells assist in the repair of injured nerves

Unlike the brain and spinal cord, the peripheral nervous system has an astonishing capacity for regeneration following injury. Researchers at the Max Planck Institute of Experimental Medicine in Göttingen have discovered that, following nerve damage, peripheral glial cells produce the growth factor neuregulin1, which makes an important contribution to the regeneration of damaged nerves.

From their cell bodies to their terminals in muscle or skin, neuronal extensions or axons in the peripheral nervous system are surrounded along their entire length by glial cells. These cells, which are known as Schwann cells, envelop the axons with an insulating sheath called myelin, which enables the rapid transmission of electrical impulses. Following injury to a peripheral nerve, the damaged axons degenerate. After a few weeks, however, they regenerate and are then recovered with myelin by the Schwann cells. For thus far unexplained reasons, however, the Schwann cells do not manage to regenerate the myelin sheaths completely. Thus the function of damaged nerves often remains permanently impaired and certain muscles remain paralysed in affected patients.

In a current research study, the scientists have succeeded in showing that the growth factor neuregulin1 supports nerve repair and the redevelopment of the myelin layer. This protein is usually produced by neurons and is localised on axons where it acts as an important signal for the maturation of Schwann cells and myelin formation. Because the axons rapidly degenerate after injury, the remaining Schwann cells lose their contact with the axons. They thus lack the neuregulin1 signal of the nervous fibres. “In the phase following nerve damage, in which the axons are missing, the Schwann cells must carry out many tasks without the help of axonal signals. If the Schwann cells cannot overcome this first major obstacle in the aftermath of nerve injury, the nerve cannot be adequately repaired,” explains Ruth Stassart, one of the study authors.

To prevent this, the Schwann cells themselves take over the production of the actual neuronal signal molecule. After nerve damage, they synthesise the neuregulin1 protein until the axons have grown again. With the help of genetically modified mice, the researchers working on this study were able to show that the neuregulin1 produced in Schwann cells is necessary for the new maturation of the Schwann cells and the regeneration of the myelin sheath after injury. “In mice that lack the neuregulin1 gene in their Schwann cells, the already incomplete nerve regeneration process is extensively impaired,” explains co-author Robert Fledrich.

The researchers would now like to examine in greater detail how the Schwann cells contribute to the complete repair of myelinated axons after nerve damage, so that this information can also be used for therapeutic purposes.

Neuroscientists pinpoint location of fear memory in amygdala

A rustle of undergrowth in the outback: it’s a sound that might make an animal or person stop sharply and be still, in the anticipation of a predator. That “freezing” is part of the fear response, a reaction to a stimulus in the environment and part of the brain’s determination of whether to be afraid of it.

A neuroscience group at Cold Spring Harbor Laboratory (CSHL) led by Assistant Professor Bo Li Ph.D., together with collaborator Professor Z. Josh Huang Ph.D., today release the results of a new study that examines the how fear responses are learned, controlled, and memorized. They show that a particular class of neurons in a subdivision of the amygdala plays an active role in these processes.

Locating fear memory in the amygdala

Previous research had indicated that structures inside the amygdalae, a pair of almond-shaped formations that sit deep within the brain and are known to be involved in emotion and reward-based behavior, may be part of the circuit that controls fear learning and memory. In particular, a region called the central amygdala, or CeA, was thought to be a passive relay for the signals relayed within this circuit.

Li’s lab became interested when they observed that neurons in a region of the central amygdala called the lateral subdivision, or CeL, “lit up” in a particular strain of mice while studying this circuit.

“Neuroscientists believed that changes in the strength of the connections onto neurons in the central amygdala must occur for fear memory to be encoded,” Li says, “but nobody had been able to actually show this.”

This led the team to further probe into the role of these neurons in fear responses and furthermore to ask the question: If the central amygdala stores fear memory, how is that memory trace read out and translated into fear responses?

To examine the behavior of mice undergoing a fear test the team first trained them to respond in a Pavlovian manner to an auditory cue. The mice began to “freeze,” a very common fear response, whenever they heard one of the sounds they had been trained to fear.

To study the particular neurons involved, and to understand them in relation to the fear-inducing auditory cue, the CSHL team used a variety of methods. One of these involved delivering a gene that encodes for a light-sensitive protein into the particular neurons Li’s group wanted to look at.

By implanting a very thin fiber-optic cable directly into the area containing the photosensitive neurons, the team was able to shine colored laser light with pinpoint accuracy onto the cells, and in this manner activate them. This is a technique known as optogenetics. Any changes in the behavior of the mice in response to the laser were then monitored.

A subset of neurons in the central amygdala controls fear expression

The ability to probe genetically defined groups of neurons was vital because there are two sets of neurons important in fear-learning and memory processes. The difference between them, the team learned, was in their release of message-carrying neurotransmitters into the spaces called synapses between neurons. In one subset of neurons, neurotransmitter release was enhanced; in another it was diminished. If measurements had been taken across the total cell population in the central amygdala, neurotransmitter levels from these two distinct sets of neurons would have been averaged out, and thus would not have been detected.

Li’s group found that fear conditioning induced experience-dependent changes in the release of neurotransmitters in excitatory synapses that connect with inhibitory neurons – neurons that suppress the activity of other neurons – in the central amygdala. These changes in the strength of neuronal connections are known as synaptic plasticity.

Particularly important in this process, the team discovered, were somatostatin-positive (SOM+) neurons. Somatostatin is a hormone that affects neurotransmitter release. Li and colleagues found that fear-memory formation was impaired when they prevent the activation of SOM+ neurons.

SOM+ neurons are necessary for recall of fear memories, the team also found. Indeed, the activity of these neurons alone proved sufficient to drive fear responses. Thus, instead of being a passive relay for the signals driving fear learning and responses in mice, the team’s work demonstrates that the central amygdala is an active component, and is driven by input from the lateral amygdala, to which it is connected.

“We find that the fear memory in the central amygdala can modify the circuit in a way that translates into action — or what we call the fear response,” explains Li.

In the future Li’s group will try to obtain a better understanding of how these processes may be altered in post-traumatic stress disorder (PTSD) and other disorders involving abnormal fear learning. One important goal is to develop pharmacological interventions for such disorders.

Li says more research is needed, but is hopeful that with the discovery of specific cellular markers and techniques such as optogenetics, a breakthrough can be made.

Poor sleep in old age prevents the brain from storing memories

The connection between poor sleep, memory loss and brain deterioration as we grow older has been elusive. But for the first time, scientists at the University of California, Berkeley, have found a link between these hallmark maladies of old age. Their discovery opens the door to boosting the quality of sleep in elderly people to improve memory.

UC Berkeley neuroscientists have found that the slow brain waves generated during the deep, restorative sleep we typically experience in youth play a key role in transporting memories from the hippocampus – which provides short-term storage for memories – to the prefrontal cortex’s longer term “hard drive.”

However, in older adults, memories may be getting stuck in the hippocampus due to the poor quality of deep ‘slow wave’ sleep, and are then overwritten by new memories, the findings suggest.

“What we have discovered is a dysfunctional pathway that helps explain the relationship between brain deterioration, sleep disruption and memory loss as we get older – and with that, a potentially new treatment avenue,” said UC Berkeley sleep researcher Matthew Walker, an associate professor of psychology and neuroscience at UC Berkeley and senior author of the study published in the journal Nature Neuroscience.

Evidence Mounts for Role of Mutated Genes in Development of Schizophrenia

Johns Hopkins researchers have identified a rare gene mutation in a single family with a high rate of schizophrenia, adding to evidence that abnormal genes play a role in the development of the disease.

The researchers, in a report published in the journal Molecular Psychiatry, say that family members with the mutation in the gene Neuronal PAS domain protein 3 (NPAS3) appear at high risk of developing schizophrenia or another debilitating mental illnesses.

Normally functioning NPAS3 regulates the development of healthy neurons, especially in a region of the brain known as the hippocampus, which appears to be affected in schizophrenia. The Johns Hopkins researchers say they have evidence that the mutation found in the family may lead to abnormal activity of NPAS3, which has implications for brain development and function.

"Understanding the molecular and biological pathways of schizophrenia is a powerful way to advance the development of treatments that have fewer side effects and work better than the treatments now available," says study leader Frederick C. Nucifora Jr., Ph.D., D.O., M.H.S., an assistant professor of psychiatry and behavioral sciences at the Johns Hopkins University School of Medicine. "We could definitely use better medicines."

Stroke Survivors with PTSD More Likely to Avoid Treatment

A new survey of stroke survivors has shown that those with post-traumatic stress disorder (PTSD) are less likely to adhere to treatment regimens that reduce the risk of an additional stroke. Researchers found that 65 percent of stroke survivors with PTSD failed to adhere to treatment, compared with 33 percent of those without PTSD. The survey also suggests that nonadherence in PTSD patients is partly explained by increased ambivalence toward medication. Among stroke survivors with PTSD, approximately one in three (38 percent) had concerns about their medications. Results of the study, led by Columbia University Medical Center researchers, are published today in the British Journal of Health Psychology.

According to data from the American Stroke Association, nearly 795,000 Americans each year suffer a new or recurrent stroke. Stroke is the fourth-leading cause of death and the top cause of disability in the United States. Survivors of strokes are often prescribed treatment regiments, including antiplatelet agents, antihypertensive agents, and statins, which help reduce the risk of subsequent strokes. Previous research has shown that PTSD triggered by medical events—which affects 18 percent of stroke survivors—may impair recovery.

“Unfortunately, too many stroke survivors are not compliant with these regimens, even though we know that adherence to post-stroke treatment regimens is one of the most important components of reducing the risk of a future stroke,” said Ian M. Kronish, MD, MPH, assistant professor of medicine (Center for Behavioral Cardiovascular Health) and one of the study’s authors.

“For those with PTSD, this study shows that concerns about medications are a significant barrier to treatment adherence. Stroke survivors should be assessed for concerns about medications and PTSD symptoms, so that interventions may be introduced as early as possible to get patients back on track to avoid future stroke events.”

Deep brain stimulation improves autistic boy’s symptoms

Electrodes implanted deep in the brain of a boy with severe autism have enabled him to live a more normal life. The treatment reduced his destructive behavior and allowed the formerly nonverbal boy to speak a few words, scientists report online January 21 in Frontiers in Human Neuroscience.

The results are the first to use brain stimulation to alleviate symptoms of autism. Scientists caution that interpreting the results broadly is impossible without larger, systematic studies, but even so neurosurgeon Ali Rezai of the Ohio State University Wexner Medical Center in Columbus calls the boys’ gains “intriguing and promising.”

The boy in the study, who was 13 at the time of his experimental surgery, suffered from severe autism symptoms: He couldn’t talk or make eye contact, woke up screaming repeatedly during the night, and habitually injured himself so badly that his parents restrained him almost constantly to protect him. Multiple rounds of psychiatric drugs failed to stave off his worsening symptoms.

In an effort to help him, doctors led by Volker Sturm of the University Hospital of Cologne in Germany implanted electrodes into the boy’s brain. Through trial and error, the doctors realized that stimulating a part of the amygdala, a brain structure important for emotions and memory, improved the boy’s symptoms. Stimulating other brain areas had no effect or worsened his symptoms.

After eight weeks of continuous electrical stimulation, the boy shifted on a clinical scale that measures irritability from “severely ill” to “moderately ill.” The boy also improved on a scale that measures autism symptoms. He began to make eye contact and was better able to control his behavior.

“Connection error” in the brains of anorexics

When people see pictures of bodies, a whole range of brain regions are active. This network is altered in women with anorexia nervosa. In a functional magnetic resonance imaging study, two regions that are important for the processing of body images were functionally more weakly connected in anorexic women than in healthy women. The stronger this “connection error” was, the more overweight the respondents considered themselves. “These alterations in the brain could explain why women with anorexia perceive themselves as fatter, even though they are objectively underweight” says Prof. Dr. Boris Suchan of the Institute of Cognitive Neuroscience at the Ruhr-Universität. Together with Prof. Dr. Dietrich Grönemeyer (University of Witten-Herdecke), Prof. Dr. Silja Vocks (University of Osnabrück) and other colleagues, the Bochum researchers report in the journal Behavioural Brain Research.

Anorexics misperceive their body shape

The researchers tested ten anorexic and fifteen healthy women of similar age. To start with, all the women judged on the computer which of several different silhouettes corresponded best to their own body shape. Ten control subjects who did not participate in the MRI scan answered the same question by matching a photo of the test subject to the right silhouette. Both healthy and anorexic women estimated their body shape differently than outsiders: healthy subjects rated themselves as thinner than the control subjects. Anorexic women on the other hand perceived themselves to be fatter than the control subjects did.

Brain areas for body perception examined with MRI

In MRI scanners, the researchers then recorded the brain activity of the 25 participants while they observed photos of bodies. Above all, they analysed the activity in the “fusiform body area” (FBA) and the “extrastriate body area” (EBA), because previous studies showed that these brain regions are critical for the perception of bodies. To this end, the neuroscientists from Bochum calculated the so-called effective connectivity between the FBA and EBA in both hemispheres. This is a measure of how much the activity in several brain areas is temporally correlated. A high degree of correlation is indicative of a strong connection.

Brains of anorexics structurally and functionally altered

The connection between the FBA and EBA was weaker in women with anorexia nervosa than in healthy women. In addition, the researchers found a negative correlation between the EBA-FBA connection in the left hemisphere and the misjudgement of body weight: the weaker the effective connectivity between the EBA and FBA was, the fatter the subjects with anorexia falsely estimated themselves to be. “In a previous study we found that there are structural changes in the brains of patients with anorexia”, says Boris Suchan. They have a lower density of nerve cells in the EBA. “The new data shows that the network for body processing is also functionally altered.” The EBA, which has a lower cell density in anorexics, is also the area that stood out in the connection analysis: it receives reduced input from the FBA. “These changes could provide a mechanism for the development of anorexia”, says Suchan.