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According to a recent Harvard University study, a tiny population of neurons near the base of the brain can cause disease symptoms such as fever, appetite loss, and warm-seeking behaviour.

When someone develops an infection, most people believe it’s the immune system going into overdrive because they experience symptoms of the body’s natural defences such as fever, chills, or exhaustion. Most people are unaware that it is the brain underlying all of this. This is what happens: The brain system communicates with the immune system to determine if the body is infected, and then it orchestrates a sequence of behavioural and physiological changes that appear as unpleasant symptoms of illness.

Long-standing issues for neuroscientists have been: How and where does this happen in the brain? The solution was found in the brains of mice by Harvard researchers Catherine Dulac and Xiaowei Zhuang.

The researchers and their partners describe identifying a tiny population of neurons at the base of the brain that may cause illness symptoms such as fever, hunger loss, and warm seeking behaviour in a recent study published in Nature.

The neurons, which have never been described before, are discovered in the hypothalamus, a portion of the brain renowned for mediating important homeostatic activities that keep the body balanced and healthy.

The researchers discovered that some neurons had receptors capable of directly sensing chemical signals from the immune system, which other neurons lack.

“It was critical for us to show this general concept that the brain can even feel these immunological conditions,” said Jessica Osterhout, a postdoctoral researcher in the Dulac Lab and the study’s main author. “Previously, this was poorly understood.”

The critical portion of the hypothalamus was discovered to be immediately close to a permeable section of the brain called the blood-brain barrier, which helps flow blood to the brain.

“What happens is that the cells of the blood-brain barrier that are in contact with the blood and the peripheral immune system become activated, and these non-neuronal cells secrete cytokines and chemokines, which in turn activate the population of neurons that we discovered,” explained Dulac, Lee, and Ezpeleta Professor of Arts and Sciences and Higgins Professor of Molecular and Cellular Biology.

The goal is that scientists may one day be able to utilise their understanding of how this mechanism works to target the process in humans and reverse it when it becomes harmful to someone’s health.

A fever, for example, is normally a good response that aids in the elimination of a disease. However, if it becomes too high, it might be harmful.

The same may be true for a reduction of appetite or a decrease in thirst, which might be advantageous at first. However, a chronic shortage of nutrition or fluids might stymie healing.

“If we know how it works, maybe we can help people who have trouble with these types of symptoms, like chemo patients or cancer patients who have a really poor appetite but there’s really nothing we can do for them,” Osterhout said.

The work began as an investigation into what is known as the fever effect in autistic patients. It’s a condition in which autistic persons experience a decrease in autism symptoms when they have symptoms of an illness, such as a fever.

The objective was to discover the neurons that cause fever and connect them to the neurons that control social behaviour.

Osterhout discovered several groups of neurons that are active when an animal is unwell. Because of their proximity to the blood-brain barrier, she focused on roughly 1,000 neurons in the ventral medial preoptic portion of the hypothalamus.

Osterhout treated mice with pro-inflammatory chemicals, lipopolysaccharide or polycytidylic acid, to identify the distinct regions of neurons that get activated. She examined the parts of the brain that were illuminated in the brain scans.

Osterhout and colleagues then employed chemo- and optogenetics, a strong and precise set of tools, to manipulate and analyse the connection between distinct neuronal populations. Using these techniques, they were able to activate or mute these neurons in the brains of mice on command and then see what happened.

The researchers discovered that by employing these techniques, they could raise mouse body temperature, boost warmth seeking behaviour, and decrease hunger. According to the paper, the neurons described project to 12 different brain locations, some of which are known to govern hunger, pain sensation, and social relationships. This shows that the cell activity here may potentially influence other illness behaviours.

During the trials, the scientists detected greater activity and activation in this group of neurons when immune system chemicals released more messages. This implies that the brain and immune system were interacting with each other via paracrine signalling at the site where they concentrated their attention — the ventral medial preoptic region and the blood-brain barrier directly adjacent to it. Paracrine signalling occurs when cells produce a signal that causes changes in neighbouring cells.

Osterhout stated that the approach broadened her understanding of how neurons function.

“As neuroscientists, we frequently think about neurons triggering other neurons and not how important these other paracrine or secretion type techniques are,” she explained. “It altered my perspective on the situation.”

The size of our primary visual cortex and the amount of brain tissue dedicated to processing visual information at certain spots in visual space, according to a group of neuroscientists, can predict how well we see. The findings suggest a novel relationship between brain anatomy and behaviour.

The study’s findings were published in the journal ‘Nature Communications.’ “We discovered that we can anticipate how well someone can see based on the unique shape of their primary visual cortex,” says main author Marc Himmelberg, a postdoctoral researcher in the Center for Neural Science and Department of Psychology at New York University.

“We can better understand what underpins variations in how people perceive and interact with their visual surroundings by demonstrating that individual diversity in the anatomy of the human visual cortex is connected to variance in visual functioning.”

The bumps and grooves on each person’s brain surface, like fingerprints, are unique. The importance of these variations, however, is not entirely known, particularly when it comes to their influence on behaviour, such as disparities in our capacity to perceive.

Himmelberg and his co-authors, NYU’s Center for Neural Science and Department of Psychology professors Jonathan Winawer and Marisa Carrasco, aimed to elucidate the importance of these brain features to how we perceive in the Nature Communications study.

The primary visual cortex (V1) organises a picture projected from the eye into a map. However, it is distorted, as are many maps, with some areas of the image being larger than others.

“Think of a subway map of New York City that makes Staten Island appear smaller than Manhattan,” Winawer adds. “The map retains some accuracy, but it enlarges locations that are likely to be of greater interest. Similarly, V1 enlarges the centre of the picture we view, i.e. where our eyes are fixated, in comparison to the periphery.”

This is due to V1 having more tissue devoted to the centre of our field of vision. Similarly, V1 enlarges places to the left and right of where our eyes are fixating in comparison to regions above or below, due to changes in cortical tissue organisation.

Findings by Neuroscientists

The scientists used functional magnetic resonance imaging (fMRI) to map the size of the primary visual cortex (or “V1”) in more than two dozen adults. The amount of V1 tissue these people had allocated to processing visual information from distinct positions in their field of view—locations to the left, right, above, and below fixation—was also assessed.

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These participants also completed a task designed to evaluate their vision quality at the same areas in their field of view as the V1 assessments. The participants differentiated between the orientations of patterns displayed on a computer screen, which was used to assess “contrast sensitivity,” or the capacity to distinguish between pictures.

Their findings demonstrated that variations in V1 surface area might predict assessments of people’s contrast sensitivity. First, persons with a high V1 showed higher overall contrast sensitivity than those with a low V1 (the largest surface area is 1,776 square millimetres [mm2] and the smallest is 832 mm2).

Second, persons whose V1 had more cortex tissue processing visual input from a specific location in their field of vision had higher levels of cortical tissue.

Second, persons with more cortical tissue dedicated to processing visual information from a given place in their field of vision had better contrast sensitivity in that region than those with less cortical tissue dedicated to the same region. Third, stronger contrast sensitivity at a certain position (e.g., left) compared to another place equidistant from fixation (e.g., above) linked to areas with more or less cortical tissue, respectively, across individuals.

“In summary,” Carrasco writes, “the more local V1 surface area allocated to encoding a given region, the better the vision at that site.” “Our findings reveal that disparities in visual perception are inexorably connected to differences in the brain’s primary visual cortex anatomy.”

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Researchers at Sweden’s Karolinska Institute believe they have figured out why those who self-injure feel less pain than others. The answer appears to be a more effective pain-modulation mechanism, a development that can help patients seeking treatment for self-harm.

The study’s findings were published in the journal Molecular Psychiatry. Most individuals want to avoid discomfort, but some, particularly teenagers and young adults, can inadvertently cause bodily harm. Self-harm is closely linked to other mental health conditions such as anxiety and depression, however not everyone suffering from such a disease participates in self-harm.

Karin Jensen”s quote

“We’ve long attempted to understand how persons who self-injure differ from others and why pain alone isn’t a sufficient deterrent,” says Karin Jensen, researcher and group head at Karolinska Institutet’s Department of Clinical Neuroscience and the study’s corresponding author. “Previous research has shown that persons who self-harm are less sensitive to pain in general, although the reasons underlying this are not entirely understood.”

The current study compared pain modulation in 41 women who had participated in self-injury at least five times in the previous year to 40 matched women who had not engaged in self-injury behaviour.

The women, aged 18 to 35, were subjected to laboratory pain tests at Karolinska University Hospital twice in 2019-2020, during which they were asked to assess the pain they felt from transitory pressure and heat stimulations. MRI scans were also used to examine their brain activity during pain.

The researchers discovered that self-harming women withstood more pain than controls on average. Brain scans indicated changes in activity across the groups as well. When compared to controls, the brain activity of women who self-injure showed stronger connections between brain regions directly engaged in pain perception and those connected to pain regulation.

Another result was that the difference in pain modulation was unrelated to how long, how frequently, or in what way the subjects participated in self-injury.

“Our findings show that efficient pain modulation is a risk factor for self-injury behaviour,” says Maria Lalouni, a researcher at Karolinska Institutet’s Department of Clinical Neuroscience and the study’s joint first author with Jens Fust, who just completed his PhD on the subject. “It also informs us more about the variations in the brains of people who self-injure, knowledge that can be utilised to improve the support offered to persons seeking care for their behaviour, as well as dialogues with patients to help them comprehend their self-injury and the need for treatment.”

The study’s limitations include the fact that women who self-injure reported greater mental comorbidities than controls. They also used more medicines, such as antidepressants, which the researchers took into account.