ANIMAL TESTING
Bats’ amazing plan B for when they can’t hear
New research reveals instant compensation strategy that other animals might share
When bats can’t hear, new research finds that these hearing-dependent animals employ a remarkable compensation strategy.
They adapt immediately and robustly, suggesting for the first time that bats’ brains are hard-wired with an ability to launch a Plan B in times of diminished hearing.
The Johns Hopkins University work, newly published in Current Biology, raises questions about whether other animals and even humans might be capable of such deft accommodations.
“Bats have this amazing flexible adaptive behavior that they can employ anytime,” said senior author Cynthia F. Moss, a Johns Hopkins neuroscientist who studies bats. “Other mammals and humans also have these adaptive circuits that they can use to help make decisions and navigate their environment but what’s striking here is that it’s very fast, almost automatic.”
All animals adapt in various ways as a response to sensory deprivation. People at a loud bar, might lean in to better hear what someone is saying. A dog might tilt its head toward a muted sound.
Here researchers wondered how hearing-dependent echolocating bats might adapt when a key auditory region in the brain was turned off.
They trained bats to fly from a platform, down a corridor, and through a window to get a treat. Researchers then had the same bats repeat the task but with a critical auditory pathway in the midbrain temporarily blocked. Disabling this brain region isn’t like plugging your ears; it’s preventing most auditory signals from reaching the deep brain. The drug-induced technique is reversible and lasts about 90 minutes.
With their hearing blocked, bats were able to navigate the course surprisingly well, even on the first try. They weren’t as agile and ran into things, but every tested bat compensated immediately and effectively.
“They struggled but managed,” Moss said.
The bats changed their flight path and vocalizations. They flew lower, oriented themselves along walls and increased both the number and length of their calls, which boosted the power of echo signals they use for navigation.
“Echolocation acts like strobes, so they were basically taking more snapshots to help them get the missing information,” said co-author Clarice A. Diebold, a former Johns Hopkins graduate student who is now a postdoctoral student at Washington University in St. Louis. “We also found that they broadened the bandwidth on these calls. These adaptations are very interesting because we’d usually see them when bats are compensating for external noise but this is an internal processing deficit.”
Although the team repeated the experiments, the compensation skills of the bats didn’t improve over time. This means the adaptation behaviors the bats employed weren’t learned; they were innate, latent and hard-wired into the bats’ brain circuitry.
“It highlights how robust the brain is to manipulation and external noise,” said co-author Jennifer Lawlor, a postdoctoral fellow at Johns Hopkins.
The team was surprised that the bats could hear at all with this region of their brain disabled. They believe bats either relied on a previously unknown auditory pathway or that unaffected neurons might support hearing in previously unknown ways.
“You’d think an animal wouldn’t be able to hear at all,” Moss said. “But it suggests that there might be multiple pathways for sound to travel to the auditory cortex.”
The team would next like to determine to what degree the findings apply to other animals and humans.
“Can this work tell us something about auditory processing and adaptive responses in humans? Moss said. “Since no one has done this, we don’t know. The findings raise important questions that will be exciting to pursue in other research models.”
Authors include Kathryne Allen, Grace Capshaw, Megan G. Humphrey, Diego Cintron-De Leon and Kishore V. Kuchibhotla, all of Johns Hopkins.
the portion of the bat's brain that was temporarily silenced during the experiment.
Credit
Johns Hopkins University
Journal
Current Biology
Protein in soy may reduce the risk of heart failure by affecting gut bacteria
Nagoya University
A research team from the Nagoya University Graduate School of Medicine has discovered a promising way to slow the progression of heart failure in mice. They fed mice a diet rich in the soybean protein, β-conglycinin (β-CG), which can support heart health by influencing gut bacteria. Their analysis revealed that the soybean protein rich diet increased the production of the short-chain fatty acids (SCFAs) in the intestine that play a role in protecting the heart. Their findings were published in Clinical Nutrition.
Many people with heart problems try to eat a nutritious diet to reduce their risk of disease. As part of a healthy diet, soybeans have long been recognized for their antioxidant and anti-inflammatory properties. Based on this, the researchers suspected that proteins in soy may help prevent heart damage.
Dr. Nozomi Furukawa and colleagues fed the soy-derived protein β-CG to mice prone to heart failure and investigated its effects on the heart. The mice showed improved heart function, less muscle thickening, and reduced scarring of the heart tissue, common problems associated with the progression of heart disease.
Analysis of bacteria in the gut identified an increase in three types of SCFA-producing bacteria (Butyricimonas, Marvinbryantia, and Anaerotruncus) as well as concentrations of SCFAs that maintain gut health (acetic acid, butyric acid, and propionic acid).).
These findings suggest that β-CG helps prevent heart damage, at least in part, by promoting the growth of SCFA-producing bacteria in the intestine. Bacteria produce SCFAs in the large intestine during the digestion of fiber and other foods. SCFAs are known to have anti-inflammatory properties and to play a role in maintaining intestinal health. However, their findings suggest they may also help protect the heart from damage caused by high blood pressure.
“An important aspect of this study is that functional soy components showed beneficial effects on the heart,” Furukawa said. “Previously, effects on obesity have been shown, but the effects on cardiovascular disease were not known. Importantly, β-CG intake increases major SCFAs and their producing bacteria as a change in the gut microbiota. These SCFAs may inhibit the progression of heart failure.”
When the researchers used antibiotics to reduce the population of these SCFA-producing microbes in mice, the protective effects of β-CG disappeared. This suggested that the gut microbiota is crucial for β-CG’s heart-protective action. To confirm this, they administered sodium propionate, one of the SCFAs, to the mice and found that it had similar effects to feeding the mice β-CG, reinforcing the idea that SCFAs are a key part in reducing heart damage.
Although the researchers performed this study on mice, the findings suggest that similar mechanisms may help treat heart failure in humans. β-CG or its derivatives could potentially be developed into therapeutic agents that help prevent or slow the progression of heart failure, offering a more natural solution to a major health problem.
“Of course, soy and its components, such as β-CG, may not be effective for all people, especially those with allergies,” Furukawa explained. “In the future, our team will focus on the structure within β-CG and investigate the detailed molecular mechanism of the increase in short-chain fatty acids that show cardioprotective effects, with the aim of developing new treatment and prevention methods.”
The researchers hope that it leads to new ways to treat heart disease through diet and gut health, highlighting the connection between what we eat and how our bodies, particularly our hearts, respond. With heart failure being one of the leading causes of death worldwide, these findings could have a lasting impact on how we maintain a healthy heart.
Journal
Clinical Nutrition
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