In Nature Communications the scientists report that when they changed the rules of a task, requiring rats to adjust from performing just one step to performing two, a pair of regions on the brain’s surface, or cortex, collaborated to update that understanding and change the rats’ behavior to fit the new regime. The anterior cingulate cortex (ACC) appeared to recognize when the rats weren’t doing enough and updated cells in the motor cortex (M2) to adjust the task behavior.

“I started this project about 7 or 8 years ago when I wanted to study decision making.” said Daigo Takeuchi, a researcher at the University of Tokyo who led the work as a postdoc at the RIKEN-MIT Laboratory for Neural Circuit Genetics at The Picower Institute directed by senior author and Picower Professor Susumu Tonegawa. “New studies were finding a role for M2. I wanted to study what upstream circuits were influencing this.”

Tripping up the second step

Takeuchi and Tonegawa traced neural circuit connections that led into M2 and found that many originated in the ACC. They began to see the ACC’s role in guiding M2’s sequential decisions when they instilled a genetic manipulation in ACC cells that allowed them to suppress their activity. This “chemogenetic” disabling of the ACC had a very specific effect. When the task rules changed so that instead of having to poke their snout into just one hole to gain a little reward, rats had to poke their nose into a sequence of two holes, the rodents with silenced ACCs took much longer to realize the rule change. Compared to rats with normal ACC activity, they failed for much longer to realize the second poke was necessary. Rats had no trouble, however, going from two steps back to just one, regardless of whether their ACC was silenced.

When the scientists chemogenetically silenced the ACC cells’ terminals in M2, they got the same results as silencing the ACC overall. They also silenced other areas of the cortex, but doing that didn’t affect the ability of the rats to notice and adjust to the rule switch. Together these manipulations confirmed that it was specifically the ACC’s connections with M2 that help the rats notice and adjust to the one-step-to-two-step change.

But what effect does the ACC have in M2? Takeuchi and his co-authors measured the electrical activity of cells in M2 as the rats played their nose-poking, rule-changing game. They found that many cells were particularly activated by different task rules (i.e. one-step or two-steps). When they silenced the ACC, though, that suppressed this rule selectivity.

Within M2 Takeuchi and the team also noticed populations of neurons that responded preferentially to positive outcomes (reward for doing the task right) and negative outcomes (not getting a reward for doing the task wrong). They found that when they silenced the ACC, this actually increased the activity of the negative-outcome encoding neurons during negative feedback, particularly for the first 10-20 rounds after the rules changed from one step to two. This correlated strongly with the timing, or “epoch,” of the rats’ worst performance.

“It seems likely the epoch-specific disruption of animals’ second-choice performance is associated with the excessive enhancement of the activity of negative outcome activated neurons caused by the ACC silencing,” they wrote in the study.

The team further confirmed that the feedback, or outcomes, stage mattered by using a different technique to silence the ACC. By engineering ACC neurons to be suppressed by flashes of light (a technique called “optogenetics”) they could precisely control when the ACC went offline. They found that if they did so after the rats made an incorrect choice when the rules switched from one poke to two, they could cause the rats to continue to err. Optogenetic silencing of the ACC after rats made a correct choice didn’t undermine their subsequent behavior.

“These results indicate that ACC neurons process error feedback information following an erroneous second response and use this information to adjust the animal’s sequential choice responses in subsequent trials,” they wrote.

Too high a threshold

The evidence painted a clear picture: When the rats needed to notice that an extra step was now required, the ACC’s job was to learn from negative feedback and signal M2 to take the second step. If the ACC wasn’t available when feedback was provided, then M2 cells that emphasize negative outcomes apparently would become especially active and the rats would fail to do the required second step for a time before finally catching on.

Why would less ACC activity somehow increase the negative outcome encoding cells’ activity in M2? Takeuchi hypothesizes that what the ACC is actually doing is stimulating inhibitory cells in M2 that normally modulate the activity of those cells. With ACC activity reduced, the negative outcome encoding M2 cells experience less inhibition. The behavioral result, he theorizes, is that the rats therefore require more evidence than they should of the rule change. The mechanism isn’t completely clear, Takeuchi acknowledged, but the rats apparently need more time to experience outcome feedback from making the right decision of taking a second step before they’ll become convinced that they are on the right track doing so.

Takeuchi said that while the results demonstrate the circuit necessary for adapting to a rule change requiring more steps in a process, it also raises some interesting new questions. Is there another circuit for noticing when a multi-step process has become a one-step process? If so, is that circuit integrated with the one discussed in this study? And if the threshold model is the right one, how exactly is it working?

The implications not only matter for understanding the neural basis of natural sequential decisions but might also for AI applications ranging from game playing or industrial work, each of which can involve tasks with multiple steps.

In addition to Takeuchi and Tonegawa, the study’s other authors are Dheeraj Roy, Shruti Muralidhar, Takashi Kawai, Andrea Bari, Chanel Lovett, Heather Sullivan and Ian Wickersham.

The RIKEN Center for Brain Science, the Howard Hughes Medical Institute, the JPB Foundation and the Human Frontier Science Program Fellowship provided funding for the study.

Seagrass — the world’s only underwater flowering plant — is not only vital for biodiversity, but also absorbs carbon dioxide, which helps to tackle climate change.

In a new paper, just published in the journal Science, Swansea University researchers argue for considering the value of seagrasses beyond carbon in the context of the UN Sustainable Development goals — the shared blueprint for achieving a better and more sustainable future. Conserving and restoring seagrass meadows actually contributes to achieving 16 out of the 17 goals.

The authors, including Dr Richard Unsworth and Dr Leanne Cullen-Unsworth, explain that the planetary emergency is driving interest in using seagrasses as a nature-based solution for climate change and biodiversity recovery.

However, seagrass sensitivity to stressors is acute, and in many places, the risk of loss and degradation persists.

Dr Unsworth, who leads the University’s team and is a founding director of marine conservation charity Project Seagrass, said: “With the increasing realisation of the planetary emergency that we face, there is growing interest in using seagrasses as a nature-based solution for greenhouse gas mitigation.

“But if the ecological state of seagrasses remains compromised, then their ability to contribute to nature-based solutions for the climate emergency and biodiversity crisis remains in doubt.”

The team’s latest research has examined the major ecological role that seagrasses play and how rethinking their conservation is critical to understanding their part in fighting our planetary emergency.

Dr Unsworth said: “Seagrasses are of fundamental importance to the planet but compared with terrestrial grasses, and even seaweeds, the body of research within seagrass is magnitudes smaller.

“However, there are substantial ecological, social, and regulatory barriers and bottlenecks to seagrass restoration and conservation because of the scale of the interventions required.

“Now advances in marine robotics, molecular ecology, remote sensing, and artificial intelligence all offer new opportunities to solve conservation problems in difficult environments at unprecedented global scales.

“It is only by looking beyond carbon and recognising the true value of seagrass meadows can we place it on a pathway to net zero loss and ultimately net gain.”

Story Source:

Materials provided by Swansea University. Note: Content may be edited for style and length.

The research team developed an allergy model in which mice inhaled pollen from ragweed plants (Ambrosia artemisiifolia) collected in different geographic locations. They found that even a small amount of pollen (a total of 180 pollen grains) is sufficient to produce an allergic reaction, much less than the high pollen concentrations found in the air during the seasonal flowering period. As a result of climate change, the European flowering season is getting longer, and the plant is able to spread to more northerly areas. Furthermore, the regional origin of the pollen determines the severity of the allergic reaction it produces. The lead researcher and coordinator of the “Atopica” project, Michelle Epstein from MedUni Vienna, explained: “Our study shows that pollen from distinct environments can differ in its aggressiveness. So not only the concentration of the pollen in the air but also intrinsic changes (from within) related to the environment could alter the pollen’s ability to sensitise and cause more severe allergic symptoms.”

Wolfram Weckwerth, Professor at the Department of Functional and Evolutionary Ecology of the University of Vienna and one of the authors, said: “We now know that environmental factors change the aggressiveness of pollen. The next steps are further characterisation of the pollen, especially at the molecular level, to unambiguously identify the mixture of allergenic components.” Anke Bellaire, a collaborator at the Department of Structural and Functional Botany at the Department of Botany and Biodiversity, University of Vienna, and also one of the authors, added: “Following these exciting results, we plan to continue ultrastructural subcellular analysis of ragweed pollen for further characterisation.”

Gerhard Karrer, professor of botany at the University of Natural Resources and Applied Life Sciences, who was part of the team that collected the pollen in Austria, said: “The control of ragweed is a major public health concern and an adaptation strategy for mitigating and managing the impacts of climate change.”

According to the researchers, there is a high probability that climate change and other environmental factors will also affect a number of other pollen-producing plants. This applied research model now provides a strategy for further studies investigating the impacts of climate change on pollen allergy.

33 million Europeans suffer from ragweed allergy

Ragweed (Ambrosia artemisiifolia) is a highly allergenic plant whose pollen causes hay fever in sensitized people and can lead to asthma. Currently, over 33 million Europeans suffer from ragweed allergy and researchers predict an increase to 77 million cases by 2060 as a result of climate change. The EU’s annual economic burden of allergic asthma is already estimated to be as much as €151 billion. Ragweed is an invasive plant that is spreading particularly rapidly in Europe in the French Rhône Valley, in northern Italy, Hungary and Croatia. The season begins in August and extends throughout autumn. However, with global warming, the season is getting longer, and warmer temperatures will encourage ragweed plants to grow in more northerly areas and at higher altitudes. A single plant can produce about a billion grains of pollen per season, and these can travel over a thousand kilometres on the wind.

It is hoped that these study results, obtained as part of the European Union’s Seventh Framework Programme, Atopica (Atopic diseases in changing climate, land use and air quality, Grant Agreement No. 282687), will pave the way for ragweed alerts and regulations aimed at allergy prevention.

Story Source:

Materials provided by Medical University of Vienna. Note: Content may be edited for style and length.

The monoclonal antibody 19A11, developed by Professor Barry Gumbiner at the University of Washington and Seattle Children’s Research Institute, binds E-cadherin, a protein that helps cells stick together, especially in epithelial layers that line the skin, the gut and other organs. Cadherins and other adhesion molecules are important for maintaining the structure of vessels and preventing cancer metastasis, as well as playing a role in inflammation and related conditions such as Crohn’s disease and inflammatory bowel disease.

Researchers have previously found that treatment with 19A11 can prevent spread of lung cancer cells in mice.

Bin Xie, graduate student in biophysics, Professor Sanjeevi Sivasankar, Department of Biomedical Engineering, and colleagues at UC Davis and in Seattle, carried out detailed studies of how 19A11 binds to E-cadherin. Using X-ray crystallography, they found that the antibody binds E-cadherin near the site where it attaches to another E-cadherin molecule. With a combination of simulations and atomic force microscopy, they showed that 19A11 has two binding modes, one of which increases the adhesive strength of E-cadherin. That increased adhesion comes from the formation of a type of chemical link called a salt bridge between the molecules.

By better understanding how this antibody can increase stickiness between cells, the researchers hope to find ways to design even more effective treatments along the same lines.

Additional authors on the paper are: Andrew Priest at UC Davis; Allison Maker, Seattle Children’s Research Institute and University of Washington; David Dranow, Jenny Phan and Thomas Edwards, Seattle Structural Genomics Center for Infectious Disease and UCB Pharma; Bart Staker and Peter Myler, Seattle Structural Genomics Center for Infectious Disease and Seattle Children’s Research Institute. The work was partly supported by grants from the NIH and used resources of the Advanced Photon Source, a U.S. Department of Energy (DOE) Office of Science User Facility operated by Argonne National Laboratory.

Story Source:

Materials provided by University of California – Davis. Original written by Andy Fell. Note: Content may be edited for style and length.

Blood samples show that children have elevated markers of inflammation, such as interleukin 6, if they were exposed to higher air pollution. Further, higher air pollution was linked to lower cardiac autonomic regulation in children, which impacts how fast the heart beats and how hard it pumps, according to the study.

In the study, published Aug. 3 date in the journal New Directions for Child and Adolescent Research, researchers looked at blood samples from more than 100 healthy children ages 9-11 in the Sacramento area where pollutants near their homes were recorded by the Environmental Protection Agency. The study was authored by Anna M. Parenteau, a doctoral student, and Camelia E. Hostinar, associate professor, both from the UC Davis Department of Psychology. The work took place at UC Davis.

These findings are important because exposure to pollutants released during wildfires has been related to numerous negative health outcomes in children, who have smaller bodies and organ systems than adults, including asthma and decreased lung function, as well as neurodevelopmental outcomes like attention deficit hyperactivity disorder, autism, and deficits in school performance and memory, researchers said.

Looked at particulates

Researchers looked at fine particulate matter data from the EPA (PM2.5) — or the fine particles that can penetrate lungs and pass into the bloodstream — finding the children’s blood contained markers of systemic inflammation. Additionally, PM2.5, which refers to particulate matter measuring 2.5 micrometers or smaller by the EPA, was linked to lower cardiac autonomic regulation assessed using an electrocardiogram. Specifically, researchers used data files maintained by the EPA, which have daily air quality summary information from each outdoor monitor in the country.

In total, 27 of the children studied had inflammation markers in their blood recorded during significant fires when their neighborhoods recorded significant levels of PM2.5 in the air. These times when fires were burning included during the Mendocino Complex Fire in 2018, which was active about 100 miles from the lab where blood was drawn. The findings were similar to those found in an earlier study, in which the blood of young primates was collected by UC Davis researchers after significant wildfires.

“By examining daily and monthly levels of particulate matter in relation to children’s inflammation and autonomic physiology, this study further demonstrates the immediate consequences of exposure to air pollution, which may increase risk of future disease,” Parenteau said. Furthermore, Parenteau added: “As climate change continues to impact children and families, it is paramount to understand the impact of environmental contaminants such as air pollution on children’s physiology.”

Previous studies with children have shown significant associations between ambient air pollution and allergic sensitization, respiratory symptoms, and ultra-structural and cellular changes to their lungs and airways, researchers said.

Researchers have found children may be especially susceptible to the effects of air pollution, given that, compared to adults, they have a higher intake of contaminants and greater lung surface area relative to their body weight.

Continued developmental research on environmental contaminants can sound the alarm about the effects of air pollution and inform policy changes that could promote long-term population health, researchers concluded.

Co-authors, all who had graduated and completed research at UC Davis during the study, include researchers from University of Trier, Germany; UC San Francisco; Whitman College; and University of Denver.

Story Source:

Materials provided by University of California – Davis. Original written by Karen Michele Nikos-Rose. Note: Content may be edited for style and length.

Publishing in the journal Science on Aug. 5, 2022, as part of a special issue on grasslands, the study contradicts years of assumptions that grasslands’ ecological development is quick and their recovery is rapid, posing new challenges to their successful restoration.

“Old growth grasslands have a unique suite of characteristics that develop over a really long time. Recovering grasslands do not have the same species or the same characteristics as they did prior to soil tilling or tree planting, and they take centuries to redevelop,” said Katharine Suding, senior author of the paper and Distinguished Professor in the Department of Ecology and Evolutionary Biology and Institute of Arctic and Alpine Research (INSTAAR) at CU Boulder. “It’s an important reminder that we need to conserve the ancient grasslands that are still intact.”

An expert in the field of North American grasslands, Suding partnered with other experts from around the world to evaluate the current state of global grassland science, conservation and restoration — from arid, prairie and coastal grasslands, to those in the tropics and savannahs.

Grasslands, which account for nearly 40% of land-based ecosystems, provide habitat for a wide diversity of animals and plants, and contribute to the livelihoods of over 1 billion people worldwide. They also provide significant carbon sequestration and biodiversity benefits, and can be more resilient than forests in the face of a quickly changing climate.

Yet over the past couple of centuries, ancient grasslands around the world have largely been converted into farmland, used to grow trees or been developed as cities expand.

The researchers found that while the destruction of these pristine grasslands can occur very quickly, complete recovery of grassland biodiversity and essential ecosystem functions occurs slowly or not at all. The findings further emphasize the importance of conserving the world’s remaining untouched grasslands.

“If you plant trees in an older grassland or till it for agriculture, you will probably never get many of the unique diversity and belowground characteristics back. It is irreversible,” said Suding.

Restoration takes time

Grasslands store the bulk of their material underground, in roots that can reach as far as 20 feet deep. This unseen physical presence is how they can store a lot of carbon — about a third of all carbon stored on land — and remain resilient to fire and other ecological disturbances. It’s also why grasslands are often underappreciated in comparison to forests. If it’s out of sight, it’s out of mind.

Grassland restoration, however, can take a page out of forests’ playbook.

“‘Old growth’ is not only a term for forests, but one that applies to grasslands as well,” said co-author Elise Buisson, who co-authored that finding in a 2015 publication.

Old growth grasslands are unique in their underground structures and biodiversity compared to newer, younger grasslands. And while these old growth ecosystems may never be fully replicated in modern-day landscapes, they provide a model for restoration efforts, said Suding.

Even a decade ago, grassland restoration focused on distributing species’ seed onto a landscape, adding grazing or fire, and stepping aside. The new analysis finds that it takes more than a hands-off approach to be successful. Instead of tossing all the ingredients into a crockpot and turning it on high, grasslands may need more of a step-by-step recipe approach to restoration.

“We should think of restoration as more of guiding a trajectory. Some species don’t come in right at the start, and the disturbance that maintains the grassland needs time to grow and be tweaked as these species get established and the soil develops,” said Suding. “These processes take time.”

For example, some plants do well reproducing from seed in, say, the upper Midwest but not in Colorado due to the drier climate. Many tropical grasses don’t spread by seed at all, instead by rhizomes and tubers underground, and are much more difficult to reestablish.

Implications for policy

The report comes a year after the start of the United Nations Decade on Ecosystem Restoration, which aims to restore degraded ecosystems around the world to increase biodiversity, help achieve the Sustainable Development Goals and the Paris Climate Agreement. At the same time, planting trees has become a popular “natural solution” around the world to remove large quantities of carbon from the atmosphere.

Yet while the UN initiative explicitly states, “planting trees on natural grassland may destroy more than it creates,” as countries make ambitious goals and commitments to ecosystem restoration this decade, Suding worries that for many, this only means planting trees.

“We would lose a huge element of the biodiversity on Earth if we planted trees in old growth grasslands,” said Suding. “I think we need to be a little bit more careful about what’s best for the globe, in terms of where to restore what.”

As climate change threatens the American West through drought, heat and wildfire, grasslands are also a resilient choice to use less water, reduce soil erosion and keep carbon in the ground over time. It’s the older, veteran grasslands that are most beneficial in this regard.

“They’re very resilient to a lot of these threats that we’re increasingly experiencing. Grasslands are resilient and can deliver well in terms of our priorities of carbon storage, water infiltration and soil health,” said Suding.