Gluten Triggers Strange Delusions in Woman with Celiac Disease

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By Sara G. Miller

Gluten has been implicated in a number of symptoms related to celiac disease that go beyond the digestive system, including rashes, anemia and headaches. But according to a recent case report, the wheat protein played a role in one woman’s severe psychosis.

The 37-year-old woman, whose case was described in the report, was studying for her Ph.D. when she started having delusions. Her symptoms began with a belief that people were talking about her as part of a conspiracy in which friends, family members and strangers were acting out scenes for her in a “game,” the doctors who treated the woman wrote in their report, published May 12 in The New England Journal of Medicine.

After making threats against her family, the patient was admitted to a psychiatric hospital and was diagnosed with a psychotic disorder, the doctors wrote. She was prescribed anti-psychotic medications to help control her symptoms, but they did not work very well, according to the report.

During the woman’s stay at the psychiatric hospital and at follow-up appointments after she was released, doctors noticed that she had several vitamin and mineral deficiencies, had lost a lot of weight and also had thyroid problems, according to the report.

These symptoms led doctors to suspect that the woman had celiac disease, said Dr. Alessio Fasano, director of the Center for Celiac Research and Treatment at Massachusetts General Hospital in Boston and one of the doctors who treated the woman. It was at that point that the doctors who wrote the case report got involved, he said.

The doctors at Massachusetts General Hospital confirmed that the woman had celiac disease, according to the report. However, her delusions led her to believe that the doctors were being “deceitful,” and she refused to follow a gluten-free diet, they wrote.

The woman lost her job, became homeless and attempted suicide, the doctors wrote. Eventually, she was rehospitalized at a psychiatric facility, where she was successfully placed on a gluten-free diet, they wrote.

When the woman was on a gluten-free diet, her symptoms improved, Fasano said. She was once again functional and aware of what gluten was doing to her, he said. She knew that being exposed to gluten caused her to lose control of her life, and she wanted people to understand that the gluten was causing this bizarre behavior, he added.

The differences between how the woman behaved on a gluten-free diet and after being exposed to gluten was like “Dr. Jekyll and Mr. Hyde,” Fasano said. “This was a bright young lady on her way to [getting] a Ph.D., and all of sudden,” something changed and she would do things that were harmful to herself and people around her, he said.

During the time the doctors were working with the woman, she inadvertently consumed gluten on several occasions, Fasano said. When this would happen, she would become completely lost, he said. But when she was gluten-free, she was well aware that she needed to avoid gluten because “she [didn’t] want to go to ‘that place,'” Fasano said.

When Fasano last saw the woman, around January 2016, he reported that she was doing very well. She was completely avoiding gluten, and her symptoms had gone away, he said. In fact, the woman was planning to participate in an experiment with her doctors so that they could study what happened to her when she consumed gluten, he said.

The plan was to do the experiment in a very controlled environment so that the patient would not do anything harmful, he said. The experiment would give the doctors the opportunity to study the inflammatory process that potentially caused these symptoms. They also planned to do some brain scans, he said.

But before the doctors could do the experiment, the woman accidentally ate some gluten, Fasano said. Her delusions returned, and she was put in jail after trying to kill her parents, he said.

https://www.livescience.com/55166-celiac-disease-gluten-psychosis.html

Why exercise won’t make you lose weight

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By Ben Tinker

There’s no shortage of things people swore to leave behind in 2018: bad jobs, bad relationships, bad habits. But chances are, you’re beginning 2019 with something you didn’t intend: a few extra pounds.

Every January, one of the top New Year’s resolutions is to lose weight. And if you’re looking to be successful, there’s something you should know: Diet is far more important than exercise — by a long shot.

“It couldn’t be more true,” nutritionist and CNN contributor Lisa Drayer said. “Basically, what I always tell people is, what you omit from your diet is so much more important than how much you exercise.”

Think of it like this: All of your “calories in” come from the food you eat and the beverages you drink, but only a portion of your “calories out” are lost through exercise.

According to Alexxai Kravitz, an investigator at the National Institute of Diabetes and Digestive and Kidney Diseases — part of the National Institutes of Health, “it’s generally accepted that there are three main components to energy expenditure”:

(1) Basal metabolic rate, the amount of energy it takes just to keep your body running (blood pumping, lungs breathing, brain functioning)

(2) Breaking down food, scientifically referred to as “diet-induced thermogenesis,” “specific dynamic action” or the “thermic effect of food”

(3) Physical activity

For most people, basal metabolic rate accounts for 60% to 80% of total energy expenditure, Kravitz said. He cited a study that defines this as “the minimal rate of energy expenditure compatible with life.” As you get older, your rate goes down, but increasing your muscle mass makes it go up.

About 10% of your calories are burned digesting the food you eat, which means roughly 10% to 30% are lost through physical activity.

“An important distinction here is that this number includes all physical activity: walking around, typing, fidgeting and formal exercise,” Kravitz said. “So if the total energy expenditure from physical activity is 10% to 30%, exercise is a subset of that number.

“The average person — professional athletes excluded — burns 5% to 15% of their daily calories through exercise,” he said. “It’s not nothing, but it’s not nearly equal to food intake, which accounts for 100% of the energy intake of the body.”

What’s more, as anyone who’s worked out a day in their life can tell you, exercising ramps up appetite — and that can sabotage even the best of intentions.

According to calculations by Harvard Medical School, a 185-pound person burns 200 calories in 30 minutes of walking at 4 miles per hour (a pace of 15 minutes per mile). You could easily undo all that hard work by eating four chocolate chip cookies, 1½ scoops of ice cream or less than two glasses of wine.

Even a vigorous cycling class, which can burn more than 700 calories, can be completely canceled out with just a few mixed drinks or a piece of cake.

“It’s so disproportionate — the amount of time that you would need to [exercise] to burn off those few bites of food,” Drayer said.

The sentiment here is that you’ve “earned” what you eat after working out, when instead — if your goal is to lose weight — you’d be better off not working out and simply eating less.

Of course, not all calories are created equal, but for simplicity’s sake, 3,500 calories equal 1 pound of fat. So to lose 1 pound a week, you should aim to cut 500 calories every day. If you drink soda, cutting that out of your diet is one of the easiest ways to get there.

“The other thing is that exercise can increase your appetite, especially with prolonged endurance exercise or with weight lifting,” Drayer said. “It’s another reason why I tell people who want to lose weight to really just focus on diet first.”

It is cliché — but also true — that slow and steady wins the race when it comes to weight loss. According to the US Centers for Disease Control and Prevention, “evidence shows that people who lose weight gradually (about 1 to 2 pounds per week) are more successful at keeping weight off.”

“All this is not to say that exercise doesn’t have its place,” Drayer said. “It’s certainly important for building strength and muscle mass and flexibility. It can help to manage diseases, including heart disease and diabetes. It can improve your mood. It can help fight depression. But although exercise can help with weight loss, diet is a much more important lifestyle factor.”

As the saying goes: Abs are made in the kitchen, not the gym.

https://www.cnn.com/2019/01/04/health/diet-exercise-weight-loss/index.html

Hunger Hormone Ghrelin Induces Overindulgence

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Ghrelin, the hormone that makes you hungry, also makes food, and food smells, irresistibly appealing. Karen Hopkin reports.

By Karen Hopkin

‘Tis the season…for overeating! But it’s not just your lack of willpower or the omnipresent holiday treats. No, you can lay some of the blame on ghrelin. Because a new study shows that ghrelin, the hormone that makes you hungry, also makes food…and food smells…irresistibly appealing. The finding appears in the journal Cell Reports. [Jung Eun Han et al, Ghrelin Enhances Food Odor Conditioning in Healthy Humans: An fMRI Study]

Ghrelin is produced in the stomach, and its levels rise before your habitual mealtimes and after you haven’t eaten for an extended period. So the hormone reminds you to put something in your belly. Injecting rats with ghrelin encourages them to eat…and people who receive a dose of ghrelin grab extra helpings from the buffet.

But how does the hormone induce overindulgence? To find out, researchers at McGill University trained volunteers to associate random images with the smell of food. For example, every time they saw a tree, they might get a whiff of freshly baked bread. At the same time, some of the subjects received ghrelin; others got only saline.

The volunteers were then ushered into an fMRI machine, where the researchers watched their brains to see which parts got turned on by different images.

Seems that in subjects under the influence of ghrelin, the brain region involved in pleasure and reward lit up only when volunteers viewed the images they associated with food aromas. Their brain pleasure centers were disinterested in images that had not been paired with food smells.

Also, when participants were then asked to rate the pleasantness of the images, the ones who’d been exposed to ghrelin gave higher grades to the food-associated pictures than did folks who got no ghrelin.

https://www.scientificamerican.com/podcast/episode/hunger-hormone-ghrelin-aids-overindulgence/

Man develops pathological generosity after a stroke

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By Bahar Gholipour

A 49-year-old man in Brazil survived a stroke but underwent a strange personality change afterward — he developed “pathological generosity,” according to a report of his case.

His willingness to give liberally to others – including people he barely knew — dramatically changed his life. He would spend his money on children he met on the street, buying them soda, candies and junk food, his wife told the doctors. Mr. A, as the man is called in the case report, became unable to manage his financial life, or resume his job as a department manager within a large corporation.

The stroke apparently left Mr. A with “excessive and persistent generosity,” the researchers, led by Dr. Leonardo Fontenelle from the Federal University of Rio de Janeiro.

“Stroke can cause a whole variety of neuropsychological and behavioral changes,” said Dr. Larry Goldstein, neurologist and director of the Stroke Center at Duke University, who wasn’t involved with the case. “Although the observation of personality change is not that unusual, this particular one is apparently novel,” he told LiveScience.

Very often, a behavior change after a stroke depends on the extent of injury and the location of the injury in the brain, Goldstein said.


How stroke affects personality

A stroke occurs when a blood clot blocks the blood supply to the brain, or when a blood vessel in the brain bursts. Brain damage caused by low oxygen supply can lead to emotional changes, most commonly depression, but strokes have also been known to cause pathological laughing or crying, or neglect syndrome, in which people don’t recognize one side of their visual field.

In Mr. A’s case, the stroke was due to bleeding in the brain, related to his high blood pressure.

Understanding exactly what change in the brain was driving Mr. A’s excessive generosity is very interesting for scientists, especially because the condition is in many respects the opposite of disorders such as hoarding and sociopathy, the researchers said.

Doctors determined Mr. A’s stroke occurred in a subcortical region, (below the cerebral cortex, where higher-level thinking occurs), and the damage could have affected brain areas associated with regulating normal behaviors.

But knowing the location of a stroke doesn’t necessarily predict the behavioral change. The networking that happens in the brain means there are often effects in areas of the brain not right next to the injury, Goldstein said.

Studies have pointed to a couple of brain structures as being involved in acts of generosity, such as anonymously donating to charities. These brain structures include the brain’s reward system, the researchers said.

A life forever changed?

Mr. A’s pathological generosity may provide new insights into which brain areas affect “the delicate balance between altruism and egoism, which make up one of the pillars of ordinary social motivation and decision making,” the researchers said.

Other instances of excessive benevolent behavior have been seen in cases of people with mania, Parkinson’s disease treated by certain medications, and forms of dementia.

When doctors carried out a psychological evaluation of Mr. A, they didn’t find any evidence of manic symptoms or dementia. Mr. A. reported being depressed, forgetful and unable to pay attention. He also showed some behaviors that have been linked to damage in the frontal lobe of the brain, including lack of persistence and planning, and impaired judgment, according to the report.

A CT scan showed blood flow to several brain regions, including areas in the frontal lobe, was low. These regions, although far from the bleed focus, are connected with it by neural pathways. The damage in these pathways might have disrupted the interplay of neural systems that underpin key dimensions of personality, the researchers said.

Mr. A was put on medication to treat his depression. After two years, he said he felt cured, and stopped the depression treatment, but his pathological generosity was unchanged. He was aware of changes in his behavior. According to the researchers, he often claimed, “I saw death from up-close, now I want to be in high spirits.”

When doctors asked whether he intended to resume his former job, he replied that he had already worked enough, and that it was now time “to enjoy life, which is too short.”

https://www.livescience.com/39416-pathological-generosity-stroke.html

How to Create a World Where No One Dies Waiting for a Transplant

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For nearly half a century, scientists have been trying to create a process for transplanting animal organs into humans, a theoretical dream that could help the hundreds of thousands of people in need of a lifesaving transplant. But the risks, specifically of transmitting the PERV virus from pigs to humans, have always been too great, stalling research — until now. In a mind-blowing talk, geneticist Luhan Yang explains a breakthrough: using CRISPR, a technique for editing genes, she and her colleagues have created pigs that don’t carry the virus, opening up the possibility of safely growing human-transplantable organs in pigs. Learn more about this cutting-edge science and how it could help solve the organ shortage crisis.

Baby’s Rare Brain Tumor Had Teeth

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When a 4-month-old boy’s head began to grow abnormally large, doctors were right to assume that something was seriously wrong. After a brain scan revealed a tumor, doctors underwent surgery to remove it. What they found was astonishing — multiple teeth forming inside of his brain due to a very specific type of brain tumor: craniopharyngioma.

The baby boy underwent brain surgery at the University Of Maryland Medical Center, where Drs. Narlin Beaty and Edward Ahn, physicians at University of Maryland Medical Center and Johns Hopkins Children’s Center, respectively, determined the boy had a craniopharyngioma, a benign brain tumor that develops near the pituitary gland. The rare brain tumor can grow to be larger than a golf ball. However, unlike other types of tumors, this one does not spread. “It’s not every day you see teeth in any type of tumor in the brain. In a craniopharyngioma, it’s unheard of,” Beaty told Live Science.

Beaty, however, said that this is not the first time that teeth have been found in a human brain, since they’ve been appeared in teratoma tumors. This was a similar case for a young woman in India. Twenty-three-year-old Nagabhushanam Siva was shocked when she found out that doctors had found two full-formed teeth in the tumor that she had, not in her brain, but in her eye. Also, in 1978, a young man named Doug Pritchard felt a sharp pain in his foot for several weeks before he decided get it checked out. Upon inspection, physicians found a tooth growing in his left foot. However, those tumors, teratomas, contain all the types of tissues found in early-human development — meaning, they have the components of a human child. In contrast, a craniopharyngioma only has one layer.

In the past, whenever scientific abnormalities were discovered, they were often unexplained and many times left untreated. “Before the modern surgical era this child would not have survived,” Beaty said. “He’s doing extremely well, all things considered, this was a big tumor right in the center of his brain.”

https://www.medicaldaily.com/doctors-find-teeth-babys-brain-tumor-plus-other-strange-places-teeth-have-been-found-270380

Possible Culprit of Fibromyalgia Found: Microglial Activation

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This combined MR/PET image highlights areas of the brain in which patients with fibromyalgia were found to have increased glial activation, compared with unaffected control volunteers. Credit: Marco Loggia, PhD, Martinos Center for Biomedical Imaging, Massachusetts General Hospital).

A study by Massachusetts General Hospital (MGH) researchers – collaborating with a team at the Karolinska Institutet in Sweden – has documented for the first time widespread inflammation in the brains of patients with the poorly understood condition called fibromyalgia. Their report has been published online in the journal Brain, Behavior and Immunity.

“We don’t have good treatment options for fibromyalgia, so identifying a potential treatment target could lead to the development of innovative, more effective therapies,” says Marco Loggia, PhD, of the MGH-based Martinos Center for Biomedical Imaging, co-senior author of the report.

“And finding objective neurochemical changes in the brains of patients with fibromyalgia should help reduce the persistent stigma that many patients face, often being told their symptoms are imaginary and there’s nothing really wrong with them.”

Characterized by symptoms including chronic widespread pain, sleep problems, fatigue, and problems with thinking and memory, fibromyalgia affects around 4 million adults in the U.S., according to the Centers for Disease Control and Prevention.

Previous research from the Karolinska group led by Eva Kosek, MD, PhD, co-senior author of the current study, suggested a potential role for neuroinflammation in the condition – including elevated levels of inflammatory proteins in the cerebrospinal fluid – but no previous study has directly visualized neuroinflammation in fibromyalgia patients.

A 2015 study by Loggia’s team used combined MR/PET scanning to document neuroinflammation – specifically activation of glial cells – in the brains of patients with chronic back pain. Hypothesizing that similar glial activation might be found in fibromyalgia patients as well, his team used the same PET radiopharmaceutical, which binds to the translocator protein (TSPO) that is overexpressed by activated glial cells, in their study enrolling 20 fibromyalgia patients and 14 control volunteers.

At the same time, Kosek’s team at Karolinska had enrolled a group of 11 patients and an equal number of control participants for a similar study with the TSPO-binding PET tracer. Since that radiopharmaceutical binds to two types of glial cells – microglia and astrocytes – they also imaged 11 patients, 6 who had the TSPO imaging and 5 others, and another 11 controls with a PET tracer that is thought to bind preferentially to astrocytes and not to microglia. At both centers, participants with fibromyalgia completed questionnaires to assess their symptoms. When the MGH team became aware of the similar investigation the Karolinska group had underway, the teams decided to combine their data into a single study.

The results from both centers found that glial activation in several regions of the brains of fibromyalgia patients was significantly greater than it was in control participants. Compared to the MGH team’s chronic back pain study, TSPO elevations were more widespread throughout the brain, which Loggia indicates corresponds to the more complex symptom patterns of fibromyalgia. TSPO levels in a structure called the cingulate gyrus – an area associated with emotional processing where neuroinflammation has been reported in patients with chronic fatigue syndrome – corresponded with patients reported levels of fatigue. The Karolinska team’s studies with the astrocyte-binding tracer found little difference between patients and controls, suggesting that microglia were primarily responsible for the increased neuro-inflammation in fibromyalgia patients.

“The activation of glial cells we observed in our studies releases inflammatory mediators that are thought to sensitize pain pathways and contribute to symptoms such as fatigue,” says Loggia, an assistant professor of Radiology at Harvard Medical School. “The ability to join forces with our colleagues at Karolinska was fantastic, because combining our data and seeing similar results at both sites gives confidence to the reliability of our results.”

This article has been republished from materials provided by Massachusetts General Hospital. Note: material may have been edited for length and content. For further information, please contact the cited source.

Reference:
Albrecht, D. S., Forsberg, A., Sandström, A., Bergan, C., Kadetoff, D., Protsenko, E., . . . Loggia, M. L. (2018). Brain glial activation in fibromyalgia – A multi-site positron emission tomography investigation. Brain, Behavior, and Immunity. doi:10.1016/j.bbi.2018.09.018

https://www.technologynetworks.com/cell-science/news/glial-activation-found-in-the-brains-of-fibromyalgia-patients-310084?utm_campaign=NEWSLETTER_TN_Breaking%20Science%20News&utm_source=hs_email&utm_medium=email&utm_content=68543465&_hsenc=p2ANqtz–8ZbNt7sDLF6bujB3qX9CeJA-hpSQwPHeSLoR5Ju1WYXA6SnOEepdO0o-J7qw_1aGB3nfwldpf30hV3pAvVi7SzJa8fw&_hsmi=68543465

Sudoku-induced seizure

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sudoku

By MANDY OAKLANDER

The patient was a 25-year-old man who had been buried by an avalanche during a ski trip and endured 15 minutes without enough oxygen, a condition called hypoxia. After, he developed involuntary muscle jerks of his mouth when he tried to talk and his legs when he tried to walk—but his arms didn’t seem to have been affected. That changed weeks later, explain the authors, the patient’s team of doctors from the University of Munich in Germany. “He was in the rehabilitation clinic, and he was bored, so he started doing Sudokus,” says co-author and neurologist Dr. Berend Feddersen. When the right-handed patient tried to solve a Sudoku puzzle, he experienced quick muscular contractions—clonic seizures—of his left arm. The seizures stopped instantly when he stopped the game.

The authors explain it as a case of reflex epilepsy: seizures that can be triggered by external stimuli like playing games, reading, doing math, touching and bathing in warm water. For this patient, Sudoku, which involves ordering numbers one through nine in a square grid, was such a trigger. Reading, writing and even math alone didn’t have an effect. But visualization-spatial tasks, in which the patient sorted numbers in ascending order, did. “When he solves Sudoku, one of his strategies is to arrange the numbers in some 3D manner,” Feddersen says. “That’s very interesting, because when I do Sudoku, I just make trial and error.”

After analyzing his brain imaging data, the patient’s doctors concluded that the oxygen deprivation caused damage throughout the brain, especially to the U-fibres found all around the brain that contribute to inhibition. “When these kinds of neurons are dying, then you have not enough inhibition, so a loss of U-fibres leads to an overactivation,” Feddersen says. “For him, luckily it was this kind of Sudkoku thing which was the activation, and not another one he does in his daily life.” When the patient stopped solving Sudoku puzzles, the seizures stopped, too. “[He] has been seizure free for more than 5 years,” the study authors write.

http://time.com/4078049/seizure-sudoku-puzzles/

New research into why elephants are so highly protected from cancer

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by Laura Elizabeth Mason

Elephants have developed a way to resist cancer, by resurrecting a ‘zombie’ gene known as leukemia inhibitory factor 6 (LIF6). Activated LIF6 responds to damaged DNA and efficiently kills cells that are destined to become cancer cells.

Cancer is a complex genetic disease that is caused by specific changes to the genes in one cell or group of cells. These genetic alterations cause the cell to divide uncontrollably. If all mammalian cells were equally susceptible to the genetic mutations that cause cancer, then theoretically the risk of developing cancer should be greater in larger animals – due to them having more cells and a longer life-span. However, previous studies have demonstrated that elephants have a lower-than-expected rate of cancer, compared to other mammals.

“Elephants get cancer far less than we’d expect based on their size, so we want to understand the genetic basis for this cancer resistance,” said senior author Vincent Lynch from the University of Chicago, in a recent press release.

“We found that elephants and their relatives have many non-functioning copies of the LIF gene, but that elephants themselves evolved a way to turn one of these copies, LIF6, back on.”

p53 wakes up LIF6

The TP53 gene is found in all animals, it codes for the protein p53, a tumor suppressor, that stops cells with damaged DNA from dividing. Unlike humans, who only have one copy of TP53, elephants have 20. An increased number of TP53 genes enhances the DNA-damage response, providing elephants with a distinct advantage – they are able to either repair the damaged cells or ‘kill off’ irreparable cells more efficiently.

In their latest study the researchers found that in response to DNA damage, LIF6 is transcriptionally upregulated by p53. LIF6 codes for a protein that rapidly translocates to the cell’s mitochondria. Once it reaches the mitochondrion it causes the outer mitochondrial membrane pore to open – leading to mitochondrial dysfunction, causing the cell to die.

The researchers plan to conduct additional studies to further define the molecular mechanisms by which LIF6 induces cell death.

The team hope their findings will aid efforts to therapeutically target cancer. “Maybe we can find ways of developing drugs that mimic the behaviors of the elephant’s LIF6 or of getting cancerous cells to turn on their existing zombie copies of the LIF gene,” concluded Lynch.

Reference
Vazquez et al. A zombie LIF gene in elephants is up-regulated by TP53 to induce apoptosis in response to DNA damage. Cell Reports. 2018. http://dx.doi.org/10.1016/j.celrep.2018.07.042

Behavior-Predicting Neural Code Identified

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Greater activation of neurons on one side of the superior colliculus versus the other signals the detection of a relevant event. Credit: James Herman, Ph.D., National Eye Institute

by Aswini Kanneganti

Perceptual choice behavior, taking action based on the information received from the senses is often described by mathematical models. Although the associated neural activity was interpreted in 2007, translating the simulated evidence to the complex biological process has been challenging. Additionally, identifying the exact code and the behavioral changes to subtle changes in the neural code had proven to be difficult to test.

Researchers at the National Eye Institute (NEI) have investigated the neurons in the superior colliculus (SC) as they have activity related to target probability and comprise an activity map of the visual field. Previous work published by the same team showed that SC neuronal activity correlates with behavior in a covert color-change detection task. So, the scientists hypothesized that SC neuronal activity would be ideal to test decision outcome when a relevant or irrelevant perturbation occurs. The findings were published today in the journal Nature Neuroscience. NEI is part of the National Institutes of Health.

In their new study, Krauzlis, Herman, and colleagues used an “accumulator threshold model” to study how neuronal activity in the superior colliculus relates to behavior. This model assumes that the information builds up over time until it hits a certain threshold, after that a person or animal makes a decision. Because individual neurons can slowly build up information in this way, Herman and Krauzlis elected to use neuronal signals (instead of the experimental stimulus) as the input for their behavior-prediction model. Two non-human primates were tested for their behavioral responses and neuronal firing patterns in response to a covert color-change detection task. The monkeys were trained to release the joystick in response to subtle saturation changes at a relevant (cued) location and ignore changes at an irrelevant (uncued) foil location.

The findings support the notion that neurons in the SC are critical players in allowing us to detect visual objects and events. This structure doesn’t help us recognize what the specific object or event is; instead, it’s the part of the brain that decides something is there at all. By comparing brain activity recorded from the right and left superior colliculi at the same time, the researchers were able to predict whether an animal saw an event. The study provides evidence that, if the difference in neuronal activity between the two sides reached a specific threshold (e.g., neurons in the right superior colliculus fired more strongly than the left), the monkey would release the lever, confirming visualization of the event. To further confirm this finding, the researchers perturbed the neural activity on one side by either inhibiting on increasing the neural tone, and the behavioral responses were altered.

“While we’ve known for a long time that the superior colliculus is involved in perception, we really wanted to know exactly how this part of the brain controls the perceptual choice, and find a way to describe that mechanism with a mathematical model,” said James Herman, Ph.D., lead author of the study.

“The superior colliculus plays a foundational role in our ability to process and detect events,” said Richard Krauzlis, Ph.D., principal investigator in the Laboratory of Sensorimotor Research at NEI and senior author of the study. “This new work not only shows that a specific population of neurons directly cause behavior but also that a commonly used mathematical model can predict behavior based on these neurons.”

One reason for using the color change stimulus, Krauzlis said, was that the superior colliculus doesn’t itself process this information. Instead, other parts of the brain process the changing color and transmit that information to the superior colliculus for a decision to be made. In essence, this simple differential threshold of neuronal activity in the superior colliculus triggers the animal to report the presence of something in the visual field.

“It’s surprising to discover that despite the sophisticated visual machinery that we have in the cerebral cortex, these evolutionarily older structures are still critical for the visual perception that we’re used to,” said Herman.

“For this sort of task, where you’re not asked to say exactly what was the thing, but you’re just saying, did it happen, then this activity in the superior colliculus seems to be both necessary and sufficient,” said Krauzlis.

While the model accurately predicted behavior based on activity in the superior colliculus, the pattern of activation of neurons in the superior colliculus and the signal threshold itself was unique to each monkey, meaning that each monkey had its behavioral signal code.

For more information on how this neural code is decoded, watch the video by Marlene Behrmann, Professor at Carnegie Mellon University.

https://www.labroots.com/trending/neuroscience/13378/behavior-predicting-neural-code-identified