Category Archives: Neuroscience

Discovery of Gene Involved in Chronic Pain Creates New Treatment Target – Neuroscience News

Summary: The absence of the NCX3 gene amplifies pain signals within the spinal cord, a new mouse study reveals. Increasing levels of NCX3 in the spinal cord helped reduce symptoms associated with chronic pain.

Source: University of Oxford

Oxford researchers have discovered a gene that regulates pain sensitization by amplifying pain signals within the spinal cord, helping them to understand an important mechanism underlying chronic pain in humans and providing a new treatment target.

Chronic pain is a common issue affecting millions of people worldwide, but why some people are more prone to it and what factors lead tochronic painare not fully understood.

It is well known that repeated stimulation, such as with a sharp pin prick, can lead to a heightened sensitivity to pain. This process is called pain wind-up and contributes to clinical pain disorders.

In a two-part study, researchers from Oxfords Nuffield Department of Clinical Neurosciences first comparedgenetic variationin samples from more than 1,000 participants from Colombia, to look for clues as to whether there were any genetic variants more common in people who experienced greater pain wind-up. They noted a significant difference in variants of one specific gene (the protein Sodium Calcium exchanger type-3, NCX3).

The researchers then undertook a series of experiments in mice, to understand how NCX3 regulates pain wind-up and whether it may be a treatment target. NCX3 was expressed in the mousespinal cordneurons that process and transmitpain signalsto the brain.

NCX3 was needed by these neurons to export the excess calcium that builds up following activity. In the absence of NCX3 the spinal cord neurons showed more activity in response to injury signals from the periphery and pain wind-up was increased.

Conversely, increasing the levels of NCX3 within the spinal cord could reduce pain in the mouse.

David Bennett, professor of neurology and neurobiology of the Nuffield Department of Clinical Neuroscience, said: This is the first time that we have been able to study pain in humans and then to directly demonstrate the mechanism behind it in mice, which provides us with a really broad understanding of the factors involved and how we can begin developing new treatments for it.

Professor Bennett added: Chronic pain is a global problem, and can be immensely debilitating. We carried out the study in Colombia because of the mixed ancestry of the population there, including Native Indian, African and European populations, which gave us a broad range of genetic diversity to look at. This makes these findings so exciting because of their potential international applications.

The findings imply that any drugs which can increase activity of NCX3 would be predicted to reducepainsensitization in humans.

Author: Press OfficeSource: University of OxfordContact: Press Office University of OxfordImage: The image is in the public domain

Original Research: Open access.Sodium-calcium exchanger-3 regulates pain wind-up: From human psychophysics to spinal mechanisms by Teodora Trendafilova et al. Neuron

Abstract

Sodium-calcium exchanger-3 regulates pain wind-up: From human psychophysics to spinal mechanisms

Repeated application of noxious stimuli leads to a progressively increased pain perception; this temporal summation is enhanced in and predictive of clinical pain disorders. Its electrophysiological correlate is wind-up, in which dorsal horn spinal neurons increase their response to repeated nociceptor stimulation.

To understand the genetic basis of temporal summation, we undertook a GWAS of wind-up in healthy human volunteers and found significant association withSLC8A3encoding sodium-calcium exchanger type 3 (NCX3).NCX3was expressed in mouse dorsal horn neurons, and mice lackingNCX3showed normal, acute pain but hypersensitivity to the second phase of the formalin test and chronic constriction injury.

Dorsal horn neurons lackingNCX3showed increased intracellular calcium following repetitive stimulation, slowed calcium clearance, and increased wind-up. Moreover, virally mediated enhanced spinal expression ofNCX3reduced central sensitization.

Our study highlights Ca2+efflux as a pathway underlying temporal summation and persistent pain, which may be amenable to therapeutic targeting.

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Discovery of Gene Involved in Chronic Pain Creates New Treatment Target - Neuroscience News

Silence for Thought: Special Interneuron Networks in the Human Brain – Neuroscience News

Summary: Human cortical networks have evolved a novel neural network that relies on abundant connections between inhibitory interneurons.

Source: Max Planck Institute

The analysis of the human brain is a central goal of neuroscience. However, for methodological reasons, research has largely focused on model organisms, in particular the mouse.

Now, neuroscientists gained novel insights on human neural circuitry using tissue obtained from neurosurgical interventions. Three-dimensional electron microscope data revealed a novel expanded network of interneurons in humans compared to mouse.

The discovery of this prominent network component in the human cortex encourages further detailed analysis of its function in health and disease.

At first glance, brains of mouse and human are surprisingly similar: the nerve cells that form our brains have very similar shapes and properties, the molecular mechanisms of electrical excitation are highly conserved, and many biophysical phenomena found in other species seem to also apply to human brains.

So, is it primarily the fact that our brains are 1,000-fold larger, house 1000-fold more nerve cells that allows us to play chess and write childrens books, which mice arguably cannot do?, asks Moritz Helmstaedter, director at the Max Planck Institute for Brain Research (Frankfurt) who led the new study published on June 23 in the journalScience.

By analyzing the neuronal networks in mice, monkeys and humans and mapping their complete structure in biopsies of brain tissue, so called connectomes, Helmstaedter and his team have discovered that human cortical networks have evolved a novel neuronal network type that is essentially absent in mice. This neuronal network relies on abundant connections between inhibitory interneurons.

Using biopsies from neurosurgical interventions, performed by neurosurgeon Hanno-Sebastian Meyer and his team at TU Munich, the researchers applied 3-dimensional electron microscopy to map about a million synapses in human brain samples.

Their data revealed, in humans, an unexpected bias of interneurons (enriched in humans) connecting with each other, while the innervation (synaptic connections) to principal neurons largely remained similar.

This suggests to us an almost ten-fold expansion of an interneuron-to-interneuron network, says Sahil Loomba, one of the studies lead authors.

Interneurons make about a fourth to a third of cortical nerve cells that behave in a very peculiar way: they are highly active, however, not to activate other neurons, rather to silence them. Just like kindergarten caretakers, or guards in the museum: their very laborious and highly energy consuming activity is to keep others peaceful, quiet, explains Helmstaedter.

Now imagine a room full of museum guards, all mutually silencing each other. This is what the human brain has developed!

But what could this mean? Theoretical work has suggested that such networks of silencers can prolong the time over which recent events can be kept in the neuronal network: expand the working memory.

In fact, it is highly plausible that longer working memory will help you deal with more complex tasks, expand your ability for reasoning, says Helmstaedter.

The new discovery suggests a first clear network innovation in humans that deserves intense further study.

He adds: It could also be a site of pathological change, and must be studied in the context of neuropsychiatric disorders. And last but not least: none of todays main AI methods uses such interneuron-to-interneuron networks.

Author: Irina EpsteinSource: Max Planck InstituteContact: Irina Epstein Max Planck InstituteImage: The image is credited to Loomba, Helmstaedter, MPI for Brain Research; Loomba et al., Science

Original Research: Closed access.Connectomic comparison of mouse and human cortex by Moritz Helmstaedter et al. Science

Abstract

Connectomic comparison of mouse and human cortex

The human cerebral cortex houses 1,000 times more neurons than the cerebral cortex of a mouse, but the possible differences in synaptic circuits between these species are still poorly understood.

We used 3-dimensional electron microscopy of mouse, macaque and human cortical samples to study their cell type composition and synaptic circuit architecture.

The 2.5-fold increase in interneurons in humans compared to mouse was compensated by a change in axonal connection probabilities and therefore did not yield a commensurate increase in inhibitory-vs-excitatory synaptic input balance on human pyramidal cells.

Rather, increased inhibition created an expanded interneuron-to-interneuron network, driven by an expansion of interneuron-targeting interneuron types and an increase in their synaptic selectivity for interneuron innervation.

These constitute key neuronal network alterations in human cortex.

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Silence for Thought: Special Interneuron Networks in the Human Brain - Neuroscience News

How the Brain Interprets Motion While in Motion – Neuroscience News

Summary: Researchers have discovered a novel neural mechanism involved in casual inference that helps the brain detect objects in motion while we are moving.

Source: University of Rochester

Imagine youre sitting on a train. You look out the window and see another train on an adjacent track that appears to be moving. But, has your train stopped while the other train is moving, or are you moving while the other train is stopped?

The same sensory experienceviewing a traincan yield two very different perceptions, leading you to feel either a sensation of yourself in motion or a sensation of being stationary while an object moves around you.

Human brains are constantly faced with such ambiguous sensory inputs. In order to resolve the ambiguity and correctly perceive the world, our brains employ a process known as causal inference.

Causal inference is a key to learning, reasoning, and decision making, but researchers currently know little about the neurons involved in the process.

In a new paper published in the journaleLife, researchers at the University of Rochester, including Greg DeAngelis, the George Eastman Professor of Brain and Cognitive Sciences, and his colleagues at Sungkyunkwan University and New York University, describe a novel neural mechanism involved in causal inference that helps thebraindetect object motion during self-motion.

The research offers new insights into how the brain interpretssensory informationand may have applications in designing artificial intelligence devices and developing treatments and therapies to treatbrain disorders.

While much has been learned previously about how the brain processesvisual motion, most laboratory studies of neurons have ignored the complexities introduced by self-motion, DeAngelis says. Under natural conditions, identifying how objects move in the world is much more challenging for the brain.

Now imagine a still, crouching lion waiting to spot prey; it is easy for the lion to spot a moving gazelle. Just like the still lion, when an observer is stationary, it is easy for her to detect when objects move in the world, because motion in the world directly maps to motion on the retina.

However, when the observer is also moving, her eyes are taking in motion everywhere on her retina as she moves relative to objects in the scene.

This causes a complex pattern of motion that makes it more difficult for the brain to detect when an object is moving in the world and when it is stationary; in this case, the brain has to distinguish between image motion that results from the observer herself versus image motion of other objects around the self.

The researchers discovered a type of neuron in the brain that has a particular combination of response properties, which makes the neuron well-suited to contribute to the task of distinguishing between self-motion and the motion of other objects.

Although the brain probably uses multiple tricks to solve this problem, this new mechanism has the advantage that it can be performed in parallel at each local region of the visual field, and thus may be faster to implement than more global processes, DeAngelis says. This mechanism might also be applicable to autonomous vehicles, which also need to rapidly detect moving objects.

Unraveling a complicated circuit of neurons

Causal inference involves a complicated circuit of neurons and other sensory mechanisms that are not widely understood, DeAngelis says, because sensory perception works so well most of the time, so we take for granted how difficult of a computational problem it is.

In actuality, sensory signals are noisy and incomplete. Additionally, there are many possible events that could happen in the world that would produce similar patterns of sensory input.

Consider a spot of light that moves across theretinaof the eye. The same visual input could be the result of a variety of situations: it could be caused by an object that moves in the world while the viewer remains stationary, such as a person standing still at a window and observing a moving ambulance with a flashing light; it could be caused by a moving observer viewing a stationary object, such as a runner noticing a lamppost from a distance; or it could be caused by many different combinations of object motion, self-motion, and depth.

The brain has a difficult problem to solve: it must infer what most likely caused the specific pattern of sensory signals that it received. It can then draw conclusions about the situation and plan appropriate actions in response.

Building on these latest results and using data science, lab experiments, computer models, and cognitive theory, DeAngelis, Haefner, and their colleagues will continue working to pinpoint single neurons and groups ofneuronsthat are involved in the process.

Their goal is to identify how the brain generates a consistent view of reality through interactions between the parts of the brain that process sensory stimuli and the parts of the brain that make decisions and plan actions.

Developing therapies and artificial intelligence

Recognizing how the brain uses causal inference to separate self-motion from object motion may help in designing artificial intelligence and autopilot devices.

Understanding how the brain infers self-motion andobject motionmight provide inspiration for improving existing algorithms for autopilot devices on planes and self-driving cars, Haefner says. For example, a planes circuitry must take into account the planes self-motionin the air while also avoiding other moving planes appearing around it.

The research may additionally have important applications in developing treatments and therapies for neural disorders such as autism and schizophrenia, conditions in which casual inference is thought to be impaired.

While the project is basic science focused on understanding the fundamental mechanisms of causal inference, this knowledge should eventually be applicable to the treatment of these disorders, DeAngelis says.

Author: Lindsey ValichSource: University of RochesterContact: Lindsey Valich University of RochesterImage: The image is in the public domain

Original Research: Open access.A neural mechanism for detecting object motion during self-motion by HyungGoo R Kim et al. eLife

Abstract

A neural mechanism for detecting object motion during self-motion

Detection of objects that move in a scene is a fundamental computation performed by the visual system. This computation is greatly complicated by observer motion, which causes most objects to move across the retinal image.

How the visual system detects scene-relative object motion during self-motion is poorly understood.

Human behavioral studies suggest that the visual system may identify local conflicts between motion parallax and binocular disparity cues to depth and may use these signals to detect moving objects.

We describe a novel mechanism for performing this computation based on neurons in macaque middle temporal (MT) area with incongruent depth tuning for binocular disparity and motion parallax cues.

Neurons with incongruent tuning respond selectively to scene-relative object motion, and their responses are predictive of perceptual decisions when animals are trained to detect a moving object during self-motion.

This finding establishes a novel functional role for neurons with incongruent tuning for multiple depth cues.

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How the Brain Interprets Motion While in Motion - Neuroscience News

Smoking Increases the Risk of Depression and Schizophrenia – Neuroscience News

Summary: New research finds smoking significantly increases the risk of a person developing schizophrenia or depression.

Source: University of Bristol

Smoking increases the risk of developing schizophrenia by between 53% and 127% and of developing depression by 54% to 132%, a report by academics from the University of Bristol published today has shown.

More research is needed to identify why this is the case, and more evidence is needed for other mental health conditions such as anxiety or bipolar disorder.

The evidence presented today at the Royal College of Psychiatrists International Congress has been shared with the government, which is currently developing a new Tobacco Control Plan for publication later this year.

The Congress will also be given new data on the numbers of smokers withmental healthconditions. Rates ofsmokingare much higher among people with mentalhealthconditions than those without, and among Englands 6 million smokers there are an estimated:

These analyses are timely as the government is currently considering recommendations by the Khan Review for the forthcoming Tobacco Control Plan to deliver its Smokefree 2030 ambition.

The independent review by Javed Khan was commissioned by the Secretary of State to help the government to identify the most impactful interventions to reduce the uptake of smoking, and support people to stop smoking, for good. One of Khans 15 recommendations was that action is needed to tackle the issue of smoking and mental health.

One of the authors of the new report Professor Marcus Munafo Professor of Biological Psychology at the University of Bristol, said: There is no longer any doubt that smoking is bad for mental health and this needs to be a priority in the forthcoming Tobacco Control Plan.

Those working with people with mental health conditions need to understand and address the vicious cycle of bidirectional effects, whereby having symptoms of mental illness causes individuals to smoke more and to be more likely to become addicted.

At the same time, smoking also increases the risk of subsequent mental illness and exacerbates mental health symptoms. Lower rates of smoking will improve overall levels of good mental health as well asphysical health.

Alongside the report a joint publication by Action on Smoking and Health (ASH) and the Royal College of Psychiatrists Public Mental Health Implementation Centre sets out how a public mental health approach to smoking can be taken to address smoking and reduce poor mental health.

The NHS has pledged to put support in place for smokers on mental health wards and those accessing support in the community, but this is largely confined to those with severe mental illness.

Dr. Adrian James, president of the Royal College of Psychiatrists said: Smoking addiction is not a trivial matter; it causes serious harm to both body and mind. Smokers with mental health conditions can quit with the right support from healthcare professionals. Its our duty as psychiatrists to offer them the help they need to succeed.

Joanne Hart, former smoker who has recovered from depression said: Stopping smoking changed my life for the better, both physically and mentally. It is shocking to learn that smoking could have been one of the reasons for my depression. As a smoker I knew I was damaging my health but when times were tough it was easy to think that it was helping mentallyeveryone should know the opposite is true.

Deborah Arnott, chief executive, ASH, said: The Khan Review is called Making Smoking Obsoletethis cannot be achieved if we ignore the more than a million smokers with mental health conditions. While the NHS has started to roll out support to quit for those withsevere mental illnessthere is little provision for those with commonmental health conditionslike depression and anxietya plan is needed.

Author: Press OfficeSource: University of BristolContact: Press Office University of BristolImage: The image is in the public domain

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Smoking Increases the Risk of Depression and Schizophrenia - Neuroscience News

‘Travel Therapy’: Could a Vacation Help Mental Health and Well-Being? – Neuroscience News

Summary: Vacations may not just be an opportunity for recreation, they may also provide mental and overall health benefits.

Source: Edith Cowen University

Many of us will have likely heard of music therapy and art therapy but what about travel therapy?

A new cross-disciplinarypaperfrom Edith Cowan University (ECU) proposes we change the way we view tourism, seeing it not just as a recreational experience but as an industry that can provide real health benefits.

The collaboration between ECUs Centre for Precision Health and School of Business and Law found many aspects of going on holiday could have a positive impact on those with mental health issues or conditions.

Lead researcherDr Jun Wensaid the diverse team of tourism, public health and marketing experts investigated how tourism could benefit those living with dementia.

Medical experts can recommend dementia treatments such as music therapy, exercise, cognitive stimulation, reminiscence therapy, sensory stimulation and adaptations to a patients mealtimes and environment, Dr Wen said.

These are all also often found when on holidays.

This research is among the first to conceptually discuss how these tourism experiences could potentially work as dementiainterventions.

Holiday fun or treatment?

Dr Wen said the varied nature of tourism meant there were many opportunities to incorporate treatments for conditions such as dementia.

For example, being in new environments and having new experiences could provide cognitive and sensory stimulation.

Exercise has been linked to mental wellbeing and travelling often involves enhanced physical activity, such as more walking, Dr Wen said.

Mealtimes are often different on holiday: theyre usually more social affairs with multiple people and family-style meals have been found to positively influence dementia patients eating behaviour.

And then theres the basics like fresh air and sunshine increasing vitamin D and serotonin levels.

Everything that comes together to represent a holistic tourism experience, makes it easy to see how patients with dementia may benefit from tourism as an intervention.

A shift in thinking

Dr Wen said COVID-19s impact on travel in recent years had raised questions about tourisms value beyond lifestyle and economic factors.

Tourism has been found to boost physical and psychological wellbeing, he said.

So, after COVID, its a good time to identify tourisms place in public health and not just for healthy tourists, but vulnerable groups.

Dr Wen said he hoped a new line of collaborative research could begin to examine how tourism can enhance the lives of people with various conditions.

Were trying to do something new in bridging tourism and health science, he said.

There will have to be more empirical research and evidence to see if tourism can become one of the medical interventions for different diseases like dementia or depression.

So, tourism is not just about traveling and having fun; we need to rethink the role tourism plays in modern society.

Author: Sam JeremicSource: Edith Cowen UniversityContact: Sam Jeremic Edith Cowen UniversityImage: The image is in the public domain

Original Research: Closed access.Tourism as a dementia treatment based on positive psychology by Jun Wen et al. Tourism Management

Abstract

Tourism as a dementia treatment based on positive psychology

No research in tourism or medicine has addressed the potential relationship between travel and the medical treatment ofdementia. Given tourisms increasingly important role in society, a cross-disciplinary team of tourism and dementia experts provide insight into the potential benefits of tourism for individuals with dementia.

This conceptual effort critically reviews the tourism and dementia literature and addresses pertinent knowledge gaps. Tourism is presented as a possible way to improve dementia patients well-being as an adjunct to non-pharmacological interventions.

Accordingly, a conceptual framework is proposed to highlight the nexus between tourism experiences and dementia interventions.

Future interdisciplinary research directions are also described.

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'Travel Therapy': Could a Vacation Help Mental Health and Well-Being? - Neuroscience News

How Different Cell Types in the Brain Work Together to Suppress Nausea – Neuroscience News

Summary: Disabling activity in an area of the brain stem called the area postrema reduces nausea, while activating this area promotes vomiting, a new study reveals. The findings could lead to the development of new therapies to curb nausea.

Source: Harvard

Nausea is a bit of a catchall sensation for the human body: the unpleasant sick feeling can hit us as a result of everything from pregnancy or a migraine to eating spoiled food or undergoing chemotherapy.

Yet despite its ubiquity, scientists still dont understand precisely hownauseaworks on a mechanistic level.

Now, a team of researchers led bycell biologistsat Harvard Medical School is making strides in deepening our understanding of thebrainpathways that control nausea.

In a study conducted in mice and published June 14 inCell Reports, the scientists described a mechanism by which inhibitory neurons in a specific brain region suppress the activity of nausea-causing excitatory neurons to tamp down nausea.

The work illuminates the basic biology of nausea. If affirmed in further studies in animals and humans, it could inform the development of better anti-nausea medications.

Mediating malaise

Nausea evolved to help us survive by prompting vomiting when we ingest toxins or contract an infection. However, nausea can become a major problem when it occurs in other contextsfor example, during pregnancy or as a side effect of treatments for cancer or diabetes. If untreated, uncontrolled vomiting can lead to electrolyte imbalances and, in rare cases, life-threatening dehydration.

Current medications for nausea associated with these conditions arent all that effective, in large part because scientists dont have a detailed understanding of how the brain produces the sensation.

We cannot really develop better treatment strategies until we know the mechanism of nausea, said lead author Chuchu Zhang, a research fellow in cell biology at HMS.

Zhang and senior author Stephen Liberles, professor of cell biology in the Blavatnik Institute at HMS, are studying a region of the brain stem called the area postrema that appears to be involved in nausea.

Earlier research found that stimulating this brain region induces vomiting, while disabling it reduces nausea, but how it plays a role in nausea was not known, so we thought this would be a good place to start, Zhang said.

In a2020 studyinNeuron, Zhang and Liberles identified excitatory neurons in the area postrema that cause nausea, along with their associated receptors. Specifically, theycharacterized neurons that express the receptor for GLP1, a protein linked toblood sugarand appetite control. This receptor, they noted, is a common target for diabetes drugs, for which nausea is a major side effect.

When neurons with GLP1 receptors were turned on, mice showed signs of nausea, and when the neurons were turned off, the nausea behaviors stopped. The team also mapped these nausea-inducing neurons, located outside theblood-brain barrier, which allows them to easily detect toxins in the blood.

Understanding what receptors are expressed in the area postrema tells us what kinds of pathways may be involved in nausea signaling, Zhang said.

One traditional approach to intervene in nausea is to block those signaling pathways using pharmacological inhibitors, Liberles added.

However, the researchers wondered if there could be another way to reduce nauseaone that focuses instead on inhibitory neurons that suppress excitatory neurons in the area postrema.

An alternative path

In the new study, the researchers explored the structure and function of inhibitory neurons in the area postrema. Mapping these neurons revealed that they form a dense network that connects with nearby excitatory neurons. When the researchers activated these inhibitory neurons, the mice stopped nausea behaviors that are typically caused by excitatory neurons.

Delving deeper, the team identified three types of inhibitory neurons in the area postrema. One of these types expresses a receptor for GIP, a small protein released by the digestive system after eating, stimulating the release of insulin to control blood sugar.

We were curious whether this population of inhibitory neurons marked by the receptor for GIP could be manipulated to suppress nausea behavior, and how that mechanism works, Zhang said.

When the researchers used GIP to activate these inhibitory neurons, inhibitory currents prompted by the chemical messenger GABA flowed to nearby excitatory neurons, reducing their activity. On a behavioral level, giving mice GIP to activate these inhibitory neurons eliminated nausea behaviors. On the flip side, when the inhibitory neurons were destroyed, mice continued to show signs of nausea, even after receiving GIP.

Because mice dont vomit, Zhang noted, the study relied on observing the presence of behaviors suggestive of nausea, such as avoiding toxic substances. Given that the same brain pathways exist in humans, the researchers say the mechanism is likely conserved.

By identifying inhibitory neurons that suppress nausea in a pharmacologically accessible brain region, we can simply engage these neurons to counteract nausea responses, Liberles explained.

The brain stem inhibitory neurons in the area postrema are potentially a great clinical target for anti-nausea drug development, Zhang added. Its definitely a new strategy for developing anti-nausea treatments.

GIP is already being studied as a potential treatment for nausea, Zhang said. In fact, preliminary research has shown that giving GIP or activating GIP receptors can reduce nausea in animals that do vomit, including ferrets, dogs, and shrews. Scientists are currently working on incorporating GIP into diabetes treatments that target GLP1 receptors, with the goal of decreasing nausea as a side effect.

Zhang and Liberles plan to continue exploring the basic biology of nausea, including how these inhibitory neurons in the brain are naturally activated, and what other brain regions are involved in controlling their activity.

The team also wants to investigate additional receptors expressed byinhibitory neurons, and the various signaling factors that engage them.

Because there are different ways to trigger nausea, there are probably different receptors and signaling factors involved that could be used as drug targets to suppress nausea. Zhang said.

We want to know more about the various nausea mechanisms so that we can develop even better treatment strategies that are tailored to specific conditions.

Author: Catherine CarusoSource: HarvardContact: Catherine Caruso HarvardImage: The image is credited to Chuchu Zhang

Original Research: Open access.A brainstem circuit for nausea suppression by Chuchu Zhang et al. Cell Reports

Abstract

A brainstem circuit for nausea suppression

Nausea is a discomforting sensation of gut malaise that remains a major clinical challenge. Several visceral poisons induce nausea through the area postrema, a sensory circumventricular organ that detects bloodborne factors.

Here, we use genetic approaches based on an area postrema cell atlas to reveal inhibitory neurons that counteract nausea-associated poison responses.

The gut hormone glucose insulinotropic peptide (GIP) activates area postrema inhibitory neurons that project locally and elicit inhibitory currents in nausea-promoting excitatory neurons through -aminobutyric acid (GABA) receptors.

Moreover, GIP blocks behavioral responses to poisons in wild-type mice, with protection eliminated by targeted area postrema neuron ablation.

These findings provide insights into the basic organization of nausea-associated brainstem circuits and reveal that area postrema inhibitory neurons are an effective pharmacological target for nausea intervention.

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How Different Cell Types in the Brain Work Together to Suppress Nausea - Neuroscience News

Helping the Brain to Heal the Gut – Neuroscience News

Summary: Researchers say using psychological interventions like CBT may help to alleviate anxiety and other symptoms associated with IBS.

Source: University of Pennsylvania

On its surface, thesubredditfor irritable bowel syndrome (IBS) is a den of tongue-in-cheek humor; its logo reimagines the classic Reddit alien gripping its gut in discomfort, scatological memes abound, and the most active members sit on the porcelain throne.

Beyond the joking veneer, however, the online community shares stories of how the disorder has tinged almost every aspect of members lives with shame and discomfort. In some cases, the resulting anxiety, depression, and avoidance can be debilitating, disabling, or even life-threatening.

Spend 10 minutes on the IBS subreddit, and there will be at least one person who is suicidal, posting to that list saying, I cant take this anymore. This has destroyed my life,' says Melissa Hunt, aclinical psychologistin Penns Department of Psychology.

This is part of why Hunt has spent almost two decades studying and treating IBS, and why she just published the second edition of her book Reclaim Your Life from IBS, which offers a proven treatment plan for those suffering with the disorder.

A year after the first edition went out of print, Hunt was finding copies selling on eBay for hundreds of dollars. In response to the demand, she wanted to provide an update that included more tools to aid in treatment as well as a review of the most recent advances in the field.

Gut-brain connection

One of the most important advances is a deepened understanding of the mechanism of IBS, which is now characterized as a disorder of the gut-brain interaction, says Hunt. Signals from the gut that might go unnoticed in individuals without IBS instead get transmitted to and interpreted by the brain as pain or the urgent need for a bowel movement. This can lead to anxiety, and the intestine, which is lined with stress hormone receptors, responds by cramping and spasming.

And then youre off to the races with this positive feedback loop of increasing hypervigilance by the brain and then hypersensitivity in the gut, says Hunt.

Symptomatically, IBS manifests as abdominal pain and either constipation, diarrhea, or alternating bouts of both, and by some estimates as many as 15% of the population struggles with some form of the disorder.

For those who are more prone to diarrhea, the anxiety around explaining frequent trips to the restroom or being too far away from a convenient restroom can lead them to avoid social situations and may ultimately manifest as agoraphobia.

People get incredibly paranoid: I cant go to a restaurant because Ill have an attack. I dont want to have to leave the table and be away from everybody, and what if the bathroom is occupied? It would be a disaster, so I should just stay home,' says Hunt. Your life gets really small really quickly.

The world-shrinking nature of the condition, paired with frequent physical discomfort, can lead to desperation. Many take extreme measures, usually in the form of dietary restrictions or multiple medications, in an attempt to reduce their symptoms.

However, even the effectiveness and side effects of many clinically prescribed interventions, such as laxatives or antibiotic treatments, can vary. For example, one diet that often works well to treat IBS symptoms, called low-FODMAP, is so restrictive that adherence is virtually impossible unless patients can prepare every meal themselves, says Hunt. Counterintuitively, this diet can harm intestinal health by starving important gut bacteria, she says.

What these treatments all share is their focus on the gut side of the gut-brain interaction. Instead, Hunt focuses on the brain. She usescognitive behavioral therapyto help patients reduce their anxiety and hypervigilance around gut sensations and encourages them to slowly expose themselves to food and situations that they associate with their individual IBS symptoms.

She also teaches them to stop catastrophizing, falling into the mental trap that the worst outcome is bound to happen. This approach actually leads to reductions in visceral hypersensitivity, allowing people to alleviate symptoms while eating whatever they want.

If half of whats going on in IBS is the way the brain is interpreting those signals, then therapy that helps you reinterpret those signals in a different way is going to help, says Hunt.

Thats why talking about it is going to change their urgent diarrhea, which is initially hard for some patients to believe.

Making treatment accessible

When Hunt initially tested andpublisheda study of a low-intensity CBT treatment with limited but active therapist involvement, she was surprised by its efficacy in reducing symptoms and improving quality of life, she says. Several peers encouraged her to pursue larger studies and publish more on the subject.

Although more studies might look more prestigious, Hunt says she felt she could reach more patients and treatment providers with a self-help book. So, she wrote the first edition, which she tested with arandomized controlled trial, the gold standard for studying a treatments effectiveness.

As in the first study, participating patients saw consistent improvements in their quality of life and IBS symptoms.

In the second edition, she explores advances in treatment made in the past decade. She added a chapter on diet, which explores recent research on restrictive diets and the ways healthy eating habits might help alleviate symptoms.

She also dives into the benefits of exercise and nonjudgmental ways for people to help motivate themselves in that arena.

Hunt says she hopes the new edition will be useful to both patients and clinicians, including gastroenterologists, and therapists.

Throughout the book, she offers more clinical anecdotes so that readers might find a case that resonates, and she ends with two mock patient stories, to show how someone might work through the text with and without a therapist.

Ultimately, Hunt says the book will give people like those on the IBS subreddit access to affordable, scientifically proven help.

The real goal of treatment for IBS is to get people their lives back, not necessarily to make the symptoms go away forever, says Hunt.

You may have GI discomfort from time to timeeveryone doesbut you can still live a very rich, meaningful life.

Author: Luis Melecio-ZambranoSource: University of PennsylvaniaContact: Luis Melecio-Zambrano University of PennsylvaniaImage: The image is in the public domain

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Helping the Brain to Heal the Gut - Neuroscience News

The Benefits of Exercise in a Pill? Science Is Closer to That Goal – Neuroscience News

Summary: Researchers have identified a molecule in the blood that is produced during exercise. The molecule, Lac-Phe, can effectively reduce food intake and obesity in mouse models.

Source: Baylor College of Medicine

Researchers at Baylor College of Medicine, Stanford School of Medicine and collaborating institutions report today in the journalNaturethat they have identified a molecule in the blood that is produced during exercise and can effectively reduce food intake and obesity in mice.

The findings improve our understanding of the physiological processes that underlie the interplay between exercise and hunger.

Regular exercise has been proven to helpweight loss, regulate appetite and improve the metabolic profile, especially for people who are overweight and obese, said co-corresponding author Dr. Yong Xu, professor of pediatricsnutrition and molecular and cellular biology at Baylor.

If we can understand the mechanism by which exercise triggers these benefits, then we are closer to helping many people improve their health.

We wanted to understand how exercise works at themolecular levelto be able to capture some of its benefits, said co-corresponding author Jonathan Long, MD, assistant professor of pathology at Stanford Medicine and an Institute Scholar of Stanford ChEM-H (Chemistry, Engineering & Medicine for Human Health).

For example, older or frail people who cannot exercise enough, may one day benefit from taking a medication that can help slow down osteoporosis, heart disease or other conditions.

Xu, Long and their colleagues conducted comprehensive analyses of blood plasma compounds from mice following intense treadmill running. The most significantly induced molecule was a modified amino acid called Lac-Phe. It is synthesized from lactate (a byproduct of strenuous exercise that is responsible for the burning sensation in muscles) and phenylalanine (an amino acid that is one of the building blocks of proteins).

In mice with diet-induced obesity (fed ahigh-fat diet), a high dose of Lac-Phe suppressed food intake by about 50% compared to control mice over a period of 12 hours without affecting their movement or energy expenditure. When administered to the mice for 10 days, Lac-Phe reduced cumulativefood intakeandbody weight(owing to loss of body fat) and improved glucose tolerance.

The researchers also identified an enzyme called CNDP2 that is involved in the production of Lac-Phe and showed that mice lacking this enzyme did not lose as much weight on an exercise regime as a control group on the same exercise plan.

Interestingly, the team also found robust elevations in plasma Lac-Phe levels following physical activity in racehorses and humans. Data from a human exercise cohort showed that sprint exercise induced the most dramatic increase in plasma Lac-Phe, followed by resistance training and then endurance training.

This suggests that Lac-Phe is an ancient and conserved system that regulates feeding and is associated withphysical activityin many animal species, Long said.

Our next steps include finding more details about how Lac-Phe mediates its effects in the body, including the brain, Xu said. Our goal is to learn to modulate this exercise pathway for therapeutic interventions.

Author: Press OfficeSource: Baylor College of MedicineContact: Press Office Baylor College of MedicineImage: The image is in the public domain

Original Research: Closed access.An exercise-inducible metabolite that suppresses feeding and obesity by Jonathan Long et al. Nature

Abstract

An exercise-inducible metabolite that suppresses feeding and obesity

Exercise confers protection against obesity, type2 diabetes and other cardiometabolic diseases. However, the molecular and cellular mechanisms that mediate the metabolic benefits of physical activity remain unclear.

Here we show that exercise stimulates the production ofN-lactoyl-phenylalanine (Lac-Phe), a blood-borne signalling metabolite that suppresses feeding and obesity.

The biosynthesis of Lac-Phe from lactate and phenylalanineoccurs in CNDP2+cells, including macrophages,monocytes and otherimmune and epithelial cells localized to diverse organs. In diet-induced obese mice, pharmacological-mediated increases in Lac-Phe reduces food intake without affecting movement or energy expenditure.

Chronic administration of Lac-Phe decreases adiposity and body weight and improves glucose homeostasis. Conversely, genetic ablation of Lac-Phe biosynthesis in mice increases food intake and obesity following exercise training.

Last, large activity-inducible increases in circulating Lac-Phe are alsoobserved in humans and racehorses, establishing this metabolite as a molecular effector associated with physical activity across multiple activity modalities and mammalian species.

These data define a conserved exercise-inducible metabolite that controls food intake and influences systemic energy balance.

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The Benefits of Exercise in a Pill? Science Is Closer to That Goal - Neuroscience News

Who Benefits From Brain Training and Why? – Neuroscience News

Summary: People who are competent at near transfer, or skilled ability at similar games, are more likely to also have far transfer skills, meaning a greater ability to focus on daily living activities.

Source: UCR

If you are skilled at playing puzzles on your smartphone or tablet, what does it say about how fast you learn new puzzles, or, more broadly, how well you can focus, say, in school or at work? Or, in the language of psychologists, does near transfer predict far transfer?

A team of psychologists at UC Riverside and UC Irvinereports inNature Human Behaviorthat people who show near transfer are more likely to show far transfer.

For a person skilled at playing a game, such as Wordle, near transfer refers to being skilled at similar games, such as a crossword puzzle. An example of far transfer for this person is better focus in daily living activities.

Some people do very well in training, such as playing a video game, but they dont show near transfer perhaps because they are using highly specific strategies, said first authorAnja Pahor, an assistant research psychologist at UCR and a project scientist in the Department of Psychology at the University of Maribor in Slovenia.

For these people, far transfer is unlikely. By better understanding why this type of memory training or intervention works for some people but not others, we can move forward with a new generation of working memory training games or use approaches that are more tailored to individuals needs.

The researchers conducted three randomized control trials involving nearly 500 participants and replicated the same finding: The extent to which people improve on untrained tasks, that is, tasks they are not familiar with (near transfer), determines whether far transfer to an abstract reasoning task is successful.

By analogy, if a person running on a treadmill in the gym (training or intervention) proceeds to be able to run faster outdoors (near transfer), then this improvement predicts whether this person would be better prepared to engage in other physical activities (far transfer), such as cycling or playing a sport.

Whether and the degree to which working memory training improves performance on untrained tasks, as in fluid intelligence, the ability to think and reason abstractly and solve problems, remains a highly debated topic. Some meta-analyses show a small but significant positive effect on fluid intelligence; others argue no evidence exists that training generalizes to fluid intelligence.

What working memory researchers get most excited about is whether there is transfer to fluid intelligence, said coauthorAaron Seitz, a professor ofpsychologyat UCR and the director of the UCRBrain Game Center for Mental Fitness and Well-Being. What we say in our paper is simple: If you get near transfer, it is very likely that you also get far transfer.

But not everybody gets near transfer for a variety of reasons, such as participants disengaging during training or because that particular training is ineffective for them. These people appear not to get far transfer.

Seitz noted that people are constantly being sold brain training games.

Some studies claim these games work; other studies claim the opposite, making it difficult to interpret the interventions, he said. Further, some of these studies have lumped together people who show near transfer with people who show no near transfer. Our paper clarifies some of this confusion.

To further explore those issues, the team has launched a large-scale citizen science project that will engage 30,000 participants in various forms of brain training. The researchers welcome anyone over 18 to participate bysigning upor learn more about their ongoing work.

Susanne Jaeggi, a professor of education at UCI and director of the UCIWorking Memory and Plasticity Laband a coauthor on the research paper, cautioned that companies claims that their games improve core cognitive functions need to be carefully evaluated.

Almost everyone has access to an app or plays a game on a computer and it is easy to get seduced by the claims of some companies, she said. If we can understand how and for whom brain training apps work, we can improve them to get more out of them than just fun. Such improved apps would be especially meaningful for older adults and certain patient groups.

Funding: The research was funded by a grant to UCR and UCI from the National Institute of Mental Health of the National Institutes of Health.

Author: Iqbal PittalwalaSource: UCRContact: Iqbal Pittalwala UCRImage: The image is credited to UCR

Original Research: Open access.Near transfer to an unrelated N-back task mediates the effect of N- back working memory training on matrix reasoning by Anja Pahor et al. Nature Human Behavior

Abstract

Near transfer to an unrelated N-back task mediates the effect of N- back working memory training on matrix reasoning

The extent to which working memory training improves performance on untrained tasks is highly controversial.

Here we address this controversy by testing the hypothesis that far transfer may depend on near transfer using mediation models in three separate randomized controlled trials (RCTs).

In all three RCTs, totalling 460 individuals, performance on untrainedN-back tasks (near transfer) mediated transfer to Matrix Reasoning (representing far transfer) despite the lack of an intervention effect in RCTs 2 and 3. UntrainedN-back performance also mediated transfer to a working memory composite, which showed a significant intervention effect (RCT 3).

These findings support a model ofN-back training in which transfer to untrainedN-back tasks gates further transfer (at least in the case of working memory at the construct level) and Matrix Reasoning.

This model can help adjudicate between the many studies and meta-analyses of working memory training that have provided mixed results but have not examined the relationship between near and far transfer on an individual-differences level.

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Who Benefits From Brain Training and Why? - Neuroscience News

How the brains of social animals synchronise and expand one another – Aeon

Humans are not the only creatures that show a refined grasp of social norms. If a group of adult male rhesus monkeys (Macaca mulatta) find themselves sitting around a turning table set with food, they will display an I scratch your back, you scratch mine ethos of reciprocity. One monkey will offer another one a piece of fruit and, whats more, will expect the gesture to be reciprocated. If the offer isnt forthcoming, the first monkey is likely to retaliate by refusing to give up anything on his turn. The monkeys also like to group together in cliques; if they see one monkey has been kind to another, they collectively show kindness to the first monkey. If youre observing, it looks like nothing so much as a group of friends buying each other rounds of drinks at a bar.

While decades of research have dispelled the myth that sociality is unique to our species, scientists are still unclear about just how individual animals retain information about the structure of the society in which theyre embedded. Are the monkeys simply copying each other and sharing food via a sophisticated form of mirroring? Or are they truly keeping track of their own and others behaviour in order to make decisions within a broader social dynamic?

Over the years, biologists have used a variety of lenses to try and answer these sorts of questions. While 19th-century naturalists looked at animal behaviour with a focus on its psychological and physiological aspects, it was only after the groundbreaking work of zoologists such as Nikolaas Tinbergen and Karl von Frisch in the 1930s that the field returned to a focus on how social behaviour might be explained in evolutionary terms.

Following the emergence of the modern discipline of ethology the study of animal behaviour weve been left with two main ways of framing enquiries into the social lives of animals. One approach takes data from observations of animals in the field, trying to understand the group dynamic by looking from the outside in. Yet this necessarily makes it hard to fathom whats happening inside an individual creatures mind. By contrast, the second approach is based on detecting an individuals brain activity, and then on trying to draw a map between patterns of neuronal spiking or firing the oscillating electrical activity that produces brain waves and how the animal acts. Yet this data comes from the inside out, and often struggles to encompass group dynamics. Both of these frames tend to capture an incomplete picture.

Now a new generation of scientists is pushing for a third, more nuanced paradigm for studying animal sociality. Known as collective neuroscience, this research programme proceeds from the idea that brains have evolved primarily to help animals exist as part of a social group rather than to solve problems per se and should be studied as such. Since embedding a brain within a social structure changes how it and other brains perform, it makes no sense to only study individual minds in isolation, because it doesnt provide the full picture. Based on the notion that intelligence is a dynamic of looping cause and effect among multiple brains, researchers are drawing on the latest neuroimaging techniques to try to obtain a more detailed understanding of multiple animals brain states as they engage in a variety of social activities. The hope is that this could lead us to answers about how animals perceive their social world, and how that perception is neurally encoded.

Beyond nonhuman animals, collective neuroscience could also help us decipher some of the complexities of human society as well. Since brains appear to work differently when placed in relationships with others, we might begin to recognise the necessity to tailor interventions to improve mental health in terms of the wider social environment, rather than focusing on individual pathologies. And, in quite a different domain, if sociality is a necessary step on the road to intelligence, its unclear whether machine-learning algorithms really stand a chance of approximating a human intellect unless theyre embedded in a rich society of other algorithms.

In mainstream approaches to cognitive neuroscience in animals, portions of the brain are labelled as relating to perception, action, memory, attention, decision, sociality. But when we examine animal behaviour through a more collective lens, we begin to see that large portions of complex brains are hungry to work in harmony with others, according to Emmanuelle Tognoli, a researcher at the Center for Complex Systems and Brain Sciences at Florida Atlantic University. Like many others, Tognoli is convinced that the brain likely evolved to deal with the informational complexity of navigating and coordinating social relationships. If thats true, cognitive neuroscience that ignores sociality is probably pointless, Tognoli believes.

Much research in cognitive science examines how one brain responds to basic stimuli such as how we work through a problem a friend is recounting, or how we remember that same conversation weeks later. But even a study looking at the dynamic between two individuals lacks certain aspects of the diversity of interactions that emerge naturally in organic, more complex social groups including attention allocation, creating subgroups, and recruiting allies, says Julia Sliwa. She is a neural-systems researcher at the Paris Brain Institute who penned a seminal paper on the need for more collective neuroscience in animal research. What she and others are trying to upend, she says, is the orthodoxy that intelligence, and in this case social intelligence of a species, derives solely from the workings of the single brain. What people have been studying so far is how groups of neurons in single brains can create information in the brain; what we also need to look at, though, is how such information is processed among and between multiple brains working together.

There appear to be neurons responsible for taking note of friends complex social behaviour

The problem with trying to vindicate this idea has largely been a technical one so far, especially for nonhuman animals. Animal neuroscience research has largely relied on attaching animals to clunky machines in a lab and encouraging them to interact within a pair. But these artificial parameters will of course distort social dynamics present in the wild. Now, though, new portable technologies such as wireless neurophysiological recording devices have made it possible to observe creatures in their natural environment, where they interact organically, and in much larger groups.

Recall our friendly macaques, the subjects of a Harvard neurosurgery study published in Science in late 2021. The researchers peered into the macaques brains with recording helmets that could track brain activity in specific neurons with great precision. They observed that each kind of interaction appeared to involve several hallmark neurons lighting up in the dorsomedial prefrontal cortex, the section of the brain that is believed to play a role in social interactions. Different neurons responded differently depending on the circumstances with some neurons firing when someone didnt give a piece of fruit and going silent when someone reciprocated, while other neurons behaved in the opposite way. There were also neurons that seemed to encode information about choices, outcomes and interactions among other monkeys who were simply being observed. In other words, there appeared to be neurons responsible for taking note of friends complex social behaviour.

The Harvard researchers pulled these observations into a neuronal map, which allowed them to anticipate whether the macaques would reciprocate or retaliate on the screen before they did so in real life. These predictions were remarkably accurate, indicating that specific neurons can represent defined pieces of social information. To establish this more decisively, the researchers also worked the other way around. They applied a very small electrical current to temporarily disrupt neuronal activity in specific parts of the monkeys brains, in order to see whether that would stop the macaques from carrying out the social actions but still leave them able to perform their other cognitive functions, such as remembering or making decisions. And, just like that, the monkeys ability to perform social actions slumped, and they failed to reciprocate as expected.

The second experiment Sliwa points to focuses on brain-to-brain synchronisation. In a pivotal study from 2010, Guillaume Dumas, assistant professor of computational psychiatry at the University of Montreal, showed that the brains of human participants mirrored each other on a neurological level when engaging in activities together, such as making funny, meaningless gestures with their hands while watching each other. Another study including Dumas involved giving one of two romantic partners a painful stimulus either alone in a room, in a room with their partner, or in a room with their partner while holding hands and monitoring the effects on brain synchronisation. Unsurprisingly, hand-holding produced the most similarity in partners brain signals, and the person in pain reported that it also eased the pain. (Other studies had already shown that the analgesic effect is much lower if youre holding hands with a stranger.)

This work has widened into other contexts. Uri Hasson, a researcher at the Princeton Neuroscience Institute, has shown that a good storyteller can induce synchronisation between her and her listeners brains (if theres shared common ground, experiences and beliefs); and, in a classroom setting, how well a students brain waves sync up with their peers can serve as a good predictor of how engaged they are, and how much they feel like they get along with the group, according to research by Suzanne Dikker, a senior research scientist at the Max Planck NYU Center for Language, Music and Emotion.

Is this phenomenon present among nonhuman animals? Neuroscientists at the University of California, Berkeley, also published a paper in Science, in which they used the collective neuroscience lens to see whether the same happens for fruit bats a sociable animal that spends most of its life in a group, huddled together in small nooks during the day, and foraging for food in groups during the night.

The bats neurons spiked in similar ways, bringing their brains quite literally onto the same wavelength

The researchers tracked bats brain activity using wireless neurophysiological recording devices as the animals flew around freely in their enclosures and talked to one another with their signature high-pitched screeches. Just like the rhesus monkey study, different patterns of neuronal firing were evident while the bats were recognising and distinguishing between the calls of different members of the group. A cry from one bat stimulated activity in one set of neurons in the listener, while a vocalisation from a different bat stimulated another set of neurons. The mapping was so clear that, when in a silent room observing only the bats brain activity on a screen, researchers could identify which bats had called out.

In addition, the study found that the whole group synchronises its brain states when engaged in communication. Their neurons spiked and oscillated in similar ways, bringing their brains quite literally onto the same wavelength. And if the bats were friendly, having spent significant time together, their brains synchronised even more strongly an effect, perhaps, similar to the finding from Dumass study of hand-holding. The same effect was observed within social subgroups; members of these cliques also had a much clearer neuronal representation when one of their number was vocalising.

The neuroscientists also experimented with playing recordings of bat sounds to some of the bats, in isolation, but this failed to provoke activity in the relevant brain areas perhaps indicating that the bats knew this wasnt a genuine social interaction. This effect could partly arise from how the animals process one anothers presence using vision and olfaction in addition to hearing. But, tantalisingly, it could also indicate that another brain needs to be present for an individuals neurons to even register the existence of a social dynamic. The social context, that is, modulates activity both within and between brains.

Theres much we still dont know. Yes, specific neurons are called into action and synchronised when two bat friends call to one another, and specific neurons light up when two monkeys share food. But whether these neurons are doing the synchronisation, the recognising, or the encoding of information about what is being communicated is still to be determined. We also dont know the extent to which social information is retained over time, or whether its just for the duration of the social activity at hand. Nonetheless, the collective neuroscience agenda has undoubtedly made strides; in most previous studies, researchers couldnt even detect why a neuron was firing or not, Sliwa says, and whether it was because the animal had recognised it was interacting with their friend or because it was interacting with another animal at all.

These preliminary studies are important pieces of a much larger puzzle, according to Sliwa. Their results corroborate the idea that its possible for scientists to discover entirely new capacities when brains are scrutinised all together. Crucially, it also means giving up the clean division between stimuli and inputs versus behaviour and outputs; rather, collective neuroscience involves reckoning with the science of complex systems, where causation is not linear but looping, and social and neuronal structures mesh in unpredictable ways.

Take a sports team. Statistics about each player can tell you a lot about whether theyre going to make good additions to the team or not, but whether the group vibes together, whether they have synchronicity, whether they work together in a group, cant be quantified by the number of their scores or assists. Yet this collective X factor can be what makes a good team into a dream team.

Collective neuroscience offers a different way of seeing neuropsychiatric conditions

In the context of social-animal neuroscience, this means looking at how individual brains both affect and are affected by the social context, rather than starting from the perspective of a single brain. A complex-systems lens would demand that we study animal neuroscience across multiple interlocking scales: starting from neurons, moving into brains and embodied organisms, then across to pairs and groups, looking all the time at how all these levels relate to one another, according to Tognoli. Cognition, in this view, is a dynamical process that happens not only within and between brains, but across a variety of biological, behavioural and social levels of organisation.

Mapping how neuronal activity relates to specific social interactions, and understanding the effects of group social dynamics on the biology of the brain, could shed light on aspects of human society, too. Collective neuroscience offers a different way of seeing neuropsychiatric conditions such as depression and schizophrenia, for example not as instances of individual dysfunctions in the brain, but as phenomena that emerge from multiple dynamic physiological and social processes. How does one get to the bottom of human cognition if we are intrinsically social beings, for whom culture has had a profound impact upon our evolution? Experiments such as the macaque study helped to identify brain areas linked to abnormal or normal social behaviour; related research in humans could yield new therapies or possibilities for intervention.

In the field of AI, embracing the collective neuroscience paradigm could mean the difference between genuine intelligence and useful, but limited, algorithms. If humans complex cognitive architecture arises from their ability to engage in social and cultural learning, computer scientists ought to take note. For example, Dumas, the computational psychiatrist behind the hand-holding study, says social interaction in AI is like dark matter in the field of physics: We know well that it exists, but we do not know how to study it directly just yet. So far, AI has been somewhat solipsistic and individualistic in seeing social cognition as a potential task, rather than as a constitutive aspect of complex cognition, Dumas says. Hes now working on creating frameworks to include this multidimensional form of social intelligence in how artificial intelligence is coded, leveraging our understanding of social learning to help machines advance towards a human-level cognition.

To tackle the challenges ahead, Sliwa reminds me, its not a matter of completely ditching single-brain neuroscience. Interactions in a network might account for much of the social intelligence we see in nonhuman animals but thats also due to their brains being able to independently analyse social interactions. Its still vital to continue to study how a single brain possesses this advanced cognitive ability, as well as how those individual brains then come to work in groups. If intelligence is about dynamic of feedback loops among multiple brains, Sliwa notes, the way we study it also needs to be a system of different looping frameworks feeding into each other a lot of loops of different levels of investigation.

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How the brains of social animals synchronise and expand one another - Aeon