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This articles talks about the fact that when rats are in a community where they are free to roam, socialise etc, they are much less likely to choose the option of opioid-laced water compared to rats that are isolated and given the option of opioids or normal water. It helps researchers understand that community might be the key to battling drug addiction.

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Dr Sederer is Adjunct Professor, Department of Epidemiology, Columbia University Mailman School of Public Health, Distinguished Psychiatrist Advisor to the New York State Office of Mental Health (OMH) and Director, Columbia Psychiatry Media.
We owe to American psychologist, Dr Bruce Alexander, the understanding that addiction is about far more than any drug. That a person, or animal in his studies, is an active ingredient in their interaction with a drug. To stand a chance beating the opioid and other drug epidemics we have, we will be far better equipped if we follow his lead.

Alexander's experiments, in the 1970s, have come to be called the "Rat Park. ¹ Researchers had already proved that when rats were placed in a cage, all alone, with no other community of rats, and offered two water bottles-one filled with water and the other with heroin or cocaine-the rats would repetitively drink from the drug-laced bottles until they all overdosed and died. Like pigeons pressing a pleasure lever, they were relentless, until their bodies and brains were overcome, and they died.

But Alexander wondered: is this about the drug or might it be related to the setting they were in? To test his hypothesis, he put rats in "rat parks," where they were among others and free to roam and play, to socialize and to have sex. And they were given the same access to the same two types of drug laced bottles. When inhabiting a "rat park," they remarkably preferred the plain water. Even when they did imbibe from the drug-filled bottle, they did so intermittently, not obsessively, and never overdosed. A social community beat the power of drugs.

I believe that the biggest problem with the powerful, ubiquitous psychoactive drugs (meaning those that work on our brains and minds), is that they are so effective. In immediate and powerful ways, they change how we feel, think, relate, and behave. Or transport us away from loneliness and isolation. That is why we use them! It is also why campaigns of "just saying no" are naÃ¯ve and ineffective, and why the dilemma of drug-taking, legal and illicit, has become one of the most dominant societal dilemmas we face in the 21st century.

The rates of overdose deaths, especially but not only from opioids, in this country continue to climb. In my earlier article, I described how prescribing clinicians can help people stay alive-until they enter an effective, individually shaped, recovery program. ² This article means to convey that there is a totally low-tech way of enabling people with addiction to (figuratively) prefer to ingest water rather than addicting drugs.

What we can do, a needed and effective approach, derives from what has Alexander taught us. Humans, not just rats, need to be part of a community, encouraged to relate and experience the support of others. This is about as basic a psychological truth as exists, yet does it find application in clinicians' offices?

How many of us, during clinical encounters with patients, focus on their families, their social communities, their sources of human contact and support?

Do we ask questions like: Who do you care about in your life? Who cares about you? When was the last time you spent time with people who are good for you-instead of those who hurt you and foster your drug taking?

These questions may lead to others, such as: Who can you call or spend time with in the next couple of days? What gives you pause in calling or making the kind of human contact needed to enable recovery? What do you imagine these people would think and feel if you did make contact? How might that encounter go-where it was not about asking for help, or money, but instead simply, and most importantly, about re-igniting their friendship, their attachment to you, and their wish for your life to go well? Their interest is one way to achieve the dignity, purpose, meaning, and life of contribution so critical to the hard work of recovery.

And so on, as the conversation may continue.

The science of medicine, with the exceptional value it attributes to symptoms, diagnoses, and evidence-based therapies, has had the unintended effect of eclipsing what we know and can do about the benefits of human interaction and attachment.

Please understand, I have been in practice for a long time. I am not naÃ¯ve about the complexities of human relationships and the fears and challenges they present. Perhaps that is one reason we eschew the questions I offer above. They open essential doors, but that means we clinicians, not just our patients, have to pass through those doors as well.

Mother Theresa, not someone often quoted in medical journals, said, "If you want to change the world, go home and love your family." I think the Beatles said the same thing. And when we see people and families who are keeping their emotional heads above the often roiling waters of everyday life, who are not compulsively imbibing on drug-laced concoctions, or pathologically gambling or playing video games and the like, we will see that they lead their lives in the light of relationships, in human parks, not alone.
Dr Sederer's most recent book, The Addiction Solution: Treating Our Dependence on Opioids and Other Drugs (Scribner, 2018), is now available in paperback. Follow him on Twitter: @askdrlloyd.
Disclosures:

The author reports no conflicts of interest concerning the subject matter of this article.

References:

1. Alexander BK, Beyerstein BL, Hadaway BF, Coombs RB. Effect of Early and later colony housing on oral ingestion of morphine in rats. Pharmacol Biochem Behav. 1981;15:571-576.

2. Sederer LI. The medical irony of the deadly opioid epidemic. Psychiatric Times. May 15, 2019. https://www.psychiatrictimes.com/substance-use-disorder/medical-irony-deadly-opioid-epidemic. Accessed May 30, 2019.

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What Does "Rat Park" Teach Us About Addiction?

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How many of us, during clinical encounters with patients, focus on their families, their social communities, their sources of human contact and support?

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'Universal' brain wave pattern discovered across primate species — including humans

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'Universal' brain wave pattern discovered across primate species — including humans

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"the distinct activity patterns may reflect how the brain consciously switches focus from one piece of information to the next."

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(Image credit: Georgi Fadejev via Getty Images)

Scientists have discovered a universal pattern of brain waves in multiple primate species, including humans.

This pattern of electrical activity is seen in the six layers of tissue that cover the outside of mammals' brains, known as the cerebral cortex. In primates, higher frequency waves of electrical activity dance through the most superficial layers while slower waves bubble in layers below.

The ubiquitousness of these brain waves was revealed in a recent study, published in January in the journal

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'Universal' brain wave pattern discovered across primate species - including humans

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Scientists have uncovered a consistent brain-wave pattern that erupts throughout the cortex in several primates, including us.

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PsyPost may be a bit more academic than required. 

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"Social anxiety might be transmissible through gut microbiota, study finds"

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"Social anxiety might be transmissible through gut microbiota, study finds"

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https://www.psypost.org/social-anxiety-might-be-transmissible-through-gut-microbiota-study-finds/

#toughweekforavegan

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Social anxiety might be transmissible through gut microbiota, study finds

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Research has revealed that mice receiving gut microbiota from individuals with social anxiety disorder showed increased sensitivity to social fear, despite normal behavior in non-social tests. This highlights the potential role of gut bacteria in influencing emotions and social behaviors.

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Article is open about a study by Aberdeen University using mice to investigate a section of DNA which affects anxiety. It explains that genes turn off and on which affects health and the study's hope to be able to understand more about the effect of being able to turn genes off and on.

The published research regarding this study indicates the focus on the effect of the gene on alcohol consumption and more specifically linked to men. The research itself may be of valuable interest in the quest to discover more about the functions of DNA but the article ignores a vast amount of information from the study cited below.

McEwan, A.R., Davidson, C., Hay, E. et al. CRISPR disruption and UK Biobank analysis of a highly conserved polymorphic enhancer suggests a role in male anxiety and ethanol intake. Mol Psychiatry 26, 2263–2276 (2021). https://doi.org/10.1038/s41380-020-0707-7

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Research identifies genetic ‘switch’ that can control anxiety

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The University of Aberdeen team hope their findings could improve the lives of anxiety patients.

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Snake venom toxins can be neutralized by a new synthetic antibody

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Snake venom toxins can be neutralized by a new synthetic antibody

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This article immediately and clearly mentions the use of testing on animals, specifically mice. Scientists injected their test animals with this new synthetic antibody after exposing them to two different snake toxins, and found that they were able to recover. While there currently is no singular antibody to cure every kind of toxin exposure, scientists are hopeful that this can lead to the development of a "universal" antibody one day.

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Meghan Rosen is a staff writer who reports on the life sciences for Science News. She earned a Ph.D. in biochemistry and molecular biology with an emphasis in biotechnology from the University of California, Davis, and later graduated from the science communication program at UC Santa Cruz.

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Snake venom toxins can be neutralized by a new synthetic antibody

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A lab-made protein protected mice from lethal doses of paralyzing toxins found in a variety of snakes, a new study reports.

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Article highlights the role mice play in developing AI to decode pain and behaviour in animals, with human application anticipated.

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Article highlights the role mice play in developing AI to decode pain and behaviour in animals, with human application anticipated.

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Back in 2013, Sandeep Robert "Bob" Datta was working in his neurobiology lab at Harvard Medical School in Boston when he made the fateful decision to send his student Alex Wiltschko to the Best Buy up the street. Wiltschko was on a mission to purchase an Xbox Kinect camera, designed to pick up players' body movements for video games like Just Dance and FIFA. He plunked down about $150 and walked out with it. The unassuming piece of consumer electronics would determine the lab's direction in the coming decade and beyond.

It also placed the team within a growing scientific movement at the intersection of artificial intelligence, neuroscience, and animal behavior-a field poised to change the way researchers use other creatures to study human health conditions. The Datta Lab is learning to track the intricate nuances of mouse movement and understand the basics of how the mammal brain creates behavior, untangling the neuroscience of different health conditions and ultimately developing new treatments for people. This area of research relies on so-called "computer vision" to analyze video footage of animals and detect behavior patterns imperceptible to the unaided eye. Computer vision can also be used to auto-detect cell types, addressing a persistent problem for researchers who study complex tissues in, for example, cancers and gut microbiomes.

In the early 2010s, Datta's lab was interrogating how smell, "the sense that is most important to most animals" and the one that mice can't survive without, drives the rodents' responses to manipulations in their environment. Human observers traditionally track mouse behavior and record their observations-how many times a mouse freezes in fear, how often it rears up to explore its enclosure, how long it spends grooming, how many marbles it buries. Datta wanted to move beyond the movements visible to the unaided eye and use video cameras to track and compute whether a rodent avoids an odor (that of predator urine, for instance) or is attracted to it (like the smell of roses). The tools available at the time-overhead 2D cameras that tracked each animal as a single point-didn't yield sufficiently detailed data.

"Even in an arena in the dark, where there's no stimuli at all, [mice] just generate these incredible behavioral dynamics-none of which are being captured by, like, a dot bouncing around on the screen," says Datta. So Wiltschko identified the Xbox Kinect camera as a potential solution. Soon after its introduction in 2010, people began hacking the hardware for science and entertainment purposes. It was fitting for Datta's lab to use it to track mice: It can record in the dark using infrared light (mice move around much more when it's darker) and can see in 3D when mounted overhead by measuring how far an object is from the sensor. This enabled Datta's team to follow the subjects when they ran around, reared up, or hunkered down. As it analyzed its initial results, it realized that the Kinect camera recorded the animals' movements with a richness that 2D cameras couldn't capture.

"That got us thinking that if we could just somehow identify regularities in the data, we might be able to identify motifs or modules of action," Datta says. Looking at the raw pixel counts from the Kinect sensor, even as compressed image files and without any sophisticated analysis, they began seeing these regularities. With or without an odor being introduced, every few hundred milliseconds, mice would switch between different types of movement-rearing, bobbing their heads, turning. For several years after the first Kinect tests, Datta and his team tried to develop software to identify and record the underlying elements of the basic components of movement the animals string together to create behavior.

But they kept hitting dead ends.

"There are many, many ways you can take data and divide it up into piles. And we tried many of those ways, many for years," Datta recalls. "And we had many, many false starts."

They tried categorizing results based on the animals' poses from single frames of video, but that approach ignored movement-"the thing that makes behavior magic," according to Datta. So they abandoned that strategy and started thinking about the smaller motions that last fractions of a second and constitute behavior, analyzing them in sequence. This was the key: the recognition that movement is both discrete and continuous, made up of units but also fluid.

So they started working with machine learning tools that would respect this dual identity. In 2020, seven years after that fateful trip to Best Buy, Datta's lab published a scientific paper describing the resulting program, called MoSeq (short for "motion sequencing," evoking the precision of genetic sequencing). In this paper, they demonstrated their technique could identify the subsecond movements, or "syllables," as they call them, that make up mouse behavior when they're strung together into sequences. By detecting when a mouse reared, paused, or darted away, the Kinect opened up new possibilities for decoding the "grammar" of animal behavior.

MoSeq

Computer visionaries

In the far corner of the Datta Lab, which still resides at Harvard Medical School, Ph.D. student Maya Jay pulls back a black curtain, revealing a small room bathed in soft reddish-orange light. To the right sit three identical assemblies made of black buckets nestled inside metal frames. Over each bucket hangs a Microsoft Xbox Kinect camera, as well as a fiber-optic cable connected to a laser light source used to manipulate brain activity. The depth-sensing function of the cameras is the crucial element at play. Whereas a typical digital video captures things like color, the images produced by the Kinect camera actually show the height of the animal off the floor, Jay says-for instance, when it bobs its head or rears up on its hind legs.

Microsoft discontinued the Xbox Kinect cameras in 2017 and has stopped supporting the gadget with software updates. But Datta's lab developed its own software packages, so it doesn't rely on Microsoft to keep the cameras running, Jay says. The lab also runs its own software for the Azure Kinect, a successor to the original Kinect that the team also employs-though it was also discontinued, in 2023. Across the lab from the Xbox Kinect rigs sits a six-camera Azure setup that records mice from all angles, including from below, to generate either highly precise 2D images incorporating data from various angles or 3D images.

In the case of MoSeq and other computer vision tools, motion recordings are often analyzed in conjunction with manipulations to the brain, where sensory and motor functions are rooted in distinct modules, and neural-activity readings. When disruptions in brain circuits, either from drugs administered in the lab or edits to genes that mice share with humans, lead to changes in behaviors, it suggests a connection between the two. This makes it possible for researchers to determine which circuits in the brain are associated with certain types of behavior, as well as how medications are working on these circuits.

In 2023, Datta's lab published two papers detailing how MoSeq can contribute to new insights into an organism's internal wiring. In one, the team found that, for at least some mice in some situations, differences in mouse behavior are influenced way more by individual variation in the brain circuits involved with exploration than by sex or reproductive cycles. In another, manipulating the neurotransmitter dopamine suggested that this chemical messenger associated with the brain's reward system supports spontaneous behavior in much the same way it influences goal-directed behaviors. The idea is that little bits of dopamine are constantly being secreted to structure behavior, contrary to the popular perception of dopamine as a momentous reward. The researchers did not compare MoSeq to human observations, but it performed comparably in another set of experiments in a paper that has yet to be published.

These studies probed some basic principles of mouse neurobiology, but many experts in this field say MoSeq and similar tools could broadly revolutionize animal and human health research in the near future.

With computer vision tools, mouse behavioral tests can run in a fraction of the time that would be required with human observers. This tech comes at a time when multiple forces are calling animal testing into question. The United States Food and Drug Administration (FDA) recently changed its rules on drug testing to consider alternatives to animal testing as prerequisites for human clinical trials. Some experts, however, doubt that stand-ins such as organs on chips are advanced enough to replace model organisms yet. But the need exists. Beyond welfare and ethical concerns, the vast majority of clinical trials fail to show benefits in humans and sometimes produce dangerous and unforeseen side effects, even after promising tests on mice or other models. Proponents say computer vision tools could improve the quality of medical research and reduce the suffering of lab animals by detecting their discomfort in experimental conditions and clocking the effects of treatments with greater sensitivity than conventional observations.

Further fueling scientists' excitement, some see computer vision tools as a means of measuring the effects of optogenetics and chemogenetics, techniques that use engineered molecules to make select brain cells turn on in response to light and chemicals, respectively. These biomedical approaches have revolutionized neuroscience in the past decade by enabling scientists to precisely manipulate brain circuits, in turn helping them investigate the specific networks and neurons involved in behavioral and cognitive processes. "This second wave of behavior quantification is the other half of the coin that everyone was missing," says Greg Corder, assistant professor of psychiatry at the University of Pennsylvania. Others agree that these computer vision tools are the missing piece to track the effects of gene editing in the lab.

"[These technologies] truly are integrated and converge," agrees Clifford Woolf, a neurobiologist at Harvard Medical School who works with his own supervised computer vision tools in his pain research.

Adult supervision recommended

But is artificial intelligence ready to take over the task of tracking animal behavior and interpreting its meaning? And is it identifying meaningful connections between behavior and neurological activity just yet?

These are the questions at the heart of a tension between supervised and unsupervised AI models. Machine learning algorithms find patterns in data at speeds and scales that would be difficult or impossible for humans. Unsupervised machine learning algorithms identify any and all motifs in datasets, whereas supervised ones are trained by humans to identify specific categories. In mouse terms, this means unsupervised AIs will flag every unique movement or behavior, but supervised ones will pinpoint only those that researchers are interested in.

The major advantage of unsupervised approaches for mouse research is that people may not notice action that takes place on the subsecond scale. "When we analyze behavior types, we often actually are based on the experimenters' judgment of the behavior type, rather than mathematical clustering," says Bing Ye, a neuroscientist at the University of Michigan whose team developed LabGym, a supervised machine learning tool for mice and other animals, including rats and fruit fly larvae. The number of behavioral clusters that can be analyzed, too, is limited by human trainers. On the other hand, he says, live experts may be the most qualified to recognize behaviors of note. For this reason, he advocates transparency: publishing training datasets, the classification parameters that a supervised algorithm learns on, with any studies. That way, if experts disagree with how a tool identifies behaviors, the publicly available data provide a solid foundation for scientific debate.

Mu Yang, a neurobiologist at Columbia University and the director of the Mouse NeuroBehavior Core, a mouse behavior testing facility, is wary of trusting AI to do the work of humans until the machines have proved reliable. She is a traditional mouse behavior expert, trained to detect the animals' subtleties with her own eyes. Yang knows that the way a rodent expresses an internal state, like fear, can change depending on its context. This is true for humans too. "Whether you're in your house or...in a dark alley in a strange city, your fear behavior will look different," Yang explains. In other words, a mouse may simply pause or it may freeze in fear, but an AI could be hard-pressed to tell the difference. One of the other challenges in tracking the animals' behaviors, she says, is that testing different drugs on them may cause them to exhibit actions that are not seen in nature. Before AIs can be trusted to track these novel behaviors or movements, machine learning programs like MoSeq need to be vetted to ensure they can reliably track good old-fashioned mouse behaviors like grooming.

Yang draws a comparison to a chef, saying that you can't win a Michelin star if you haven't proved yourself as a short-order diner cook. "If I haven't seen you making eggs and pancakes, you can talk about caviar and Kobe beef all you want, I still don't know if I trust you to do that."

For now, as to whether MoSeq can make eggs and pancakes, "I don't know how you'd know," Datta says. "We've articulated some standards that we think are useful. MoSeq meets those benchmarks."

Putting the tech to the test

There are a couple of ways, Datta says, to determine benchmarks-measures of whether an unsupervised AI is correctly or usefully describing animal behavior. "One is by asking whether or not the content of the behavioral description that you get [from AI] does better or worse at allowing you to discriminate among [different] patterns of behavior that you know should occur." His team did this in the first big MoSeq study: It gave mice different medicines and used the drugs' expected effects to determine whether MoSeq was capturing them. But that's a pretty low bar, Datta admits-a starting point. "There are very few behavioral characterization methods that wouldn't be able to tell a mouse on high-dose amphetamine from a control."

The real benchmark of these tools, he says, will be whether they can provide insight into how a mouse's brain organizes behavior. To put it another way, the scientifically useful descriptions of behavior will predict something about what's happening in the brain.

Explainability, the idea that machine learning will identify behaviors experts can link to expected behaviors, is a big advantage of supervised algorithms, says Vivek Kumar, associate professor at the biomedical research nonprofit Jackson Laboratory, one of the main suppliers of lab mice. His team used this approach, but he sees training supervised classifiers after unsupervised learning as a good compromise. The unsupervised learning can reveal elements that human observers may miss, and then supervised classifiers can take advantage of human judgment and knowledge to make sure that what an algorithm identifies is actually meaningful.

"It's not magic"

MoSeq isn't the first or only computer vision tool under development for quantifying animal behavior. In fact, the field is booming as AI tools become more powerful and easier to use. We already mentioned Bing Ye and LabGym; the lab of Eric Yttri at Carnegie Mellon University has developed B-SOiD; the lab of Mackenzie Mathis at École Polytechnique Fédérale de Lausanne has DeepLabCut; and the Jackson Laboratory is developing (and has patented) its own computer vision tools. Last year Kumar and his colleagues used machine vision to develop a frailty index for mice, an assessment that is notoriously sensitive to human error.

Each of these automated systems has proved powerful in its own way. For example, B-SOiD, which is unsupervised, identified the three main types of mouse grooming without being trained in these basic behaviors.

"That's probably a good benchmark," Yang says. "I guess you can say, like the egg and pancake."

Mathis, who developed DeepLabCut, emphasizes that carefully picking data sources is critical for making the most of these tools. "It's not magic," she says. "It can make mistakes, and your trained neural networks are only as good as the data you give [them]."

And while the toolmakers are still honing their technologies, even more labs are hard at work deploying them in mouse research with specific questions and targets in mind. Broadly, the long-term goal is to aid in the discovery of drugs that will treat psychiatric and neurological conditions.

Some have already experienced vast improvements in running their experiments. One of the problems of traditional mouse research is that animals are put through unnatural tasks like running mazes and taking object recognition tests that "ignore the intrinsic richness" of behavior, says Cheng Li, professor of anesthesiology at Tongji University in Shanghai. His team found that feeding MoSeq videos of spontaneous rodent behavior along with more traditional task-oriented behaviors yielded a detailed description of the mouse version of postoperative delirium, the most common central nervous system surgical complication among elderly people.

Meanwhile, LabGym is being used to study sudden unexpected death in epilepsy in the lab of Bill Nobis at Vanderbilt University Medical Center. After being trained on videos of mouse seizures, the program detects them "every time," Nobis says.

Easing their pain

Computer vision has also become a major instrument for pain research, helping to untangle the brain's pathways involved in different types of pain and treat human ailments with new or existing drugs. And despite the FDA rule change in early 2023, the total elimination of animal testing is unlikely, Woolf says, especially in developing novel medicines. By detecting subtle behavioral signs of pain, computer vision tools stand to reduce animal suffering. "We can monitor the changes in them and ensure that we're not producing an overwhelming, painful situation-all we want is enough pain that we can measure it," he explains. "We would not do anything to a mouse that we wouldn't do to a human, in general."

His team used supervised machine learning to track behavioral signatures of pain in mice and show when medications have alleviated their discomfort, according to a 2022 paper in the journal Pain. One of the problems with measuring pain in lab animals, rather than humans, is that the creatures can't report their level of suffering, Woolf says. Scientists long believed that, proportional to body weight, the amount of medicine required to relieve pain is much higher in mice than in humans. But it turns out that if your computer vision algorithms can measure the sensation relatively accurately-and Woolf says his team's can-then you actually detect signs of pain relief at much more comparable doses, potentially reducing the level of pain inflicted to conduct this research. Measuring pain and assessing pain medicine in lab animals is so challenging that most large pharmaceutical companies have abandoned the area as too risky and expensive, he adds. "We hope this new approach is going to bring them back in."

Corder's lab at the University of Pennsylvania is working on pain too, but using the unsupervised B-SOiD in conjunction with DeepLabCut. In unpublished work, the team had DeepLabCut visualize mice as skeletal stick figures, then had B-SOiD identify 13 different pain-related behaviors like licking or biting limbs. Supervised machine learning will help make his team's work more reliable, Corder says, as B-SOiD needs instruction to differentiate these behaviors from, say, genital licking, a routine hygiene behavior. (Yttri, the co-creator of B-SOiD, says supervision will be part of the new version of his software.)

As computer vision tools continue to evolve, they could even help reduce the number of animals required for research, says FDA spokesperson Lauren-Jei McCarthy. "The agency is very much aligned with efforts to replace, reduce, or refine animal studies through the use of appropriately validated technologies."

If you build it, they will come

MoSeq's next upgrade, which has been submitted to an academic journal and is under review, will try something similar to what Corder's lab did: It will meld its unsupervised approach with keypoint detection, a computer vision method that highlights crucial points in an object like the body of a mouse. This particular approach employs the rig of six Kinect Azure cameras instead of the Datta lab's classic Xbox Kinect camera rigs.

An advantage of this approach, Datta says, is that it can be applied to existing 2D video, meaning that all the petabytes of archival mouse data from past experiments could be opened up to analysis without the cost of running new experiments on mice. "That would be huge," Corder agrees.

Datta's certainty increases as he rattles off some of his team's accomplishments with AI and mouse behavior in the past few years. "Can we use MoSeq to identify genetic mutants and distinguish them from wild types? -mice with genetics as they appear in nature. This was the subject of a 2020 paper in Nature Neuroscience, which showed that the algorithm can accurately discern mice with an autism-linked gene mutation from those with typical genetics. "Can we make predictions about neural activity?" The Datta Lab checked this off its bucket list just this year in its dopamine study. Abandoning the hedging so typical of scientists, he confidently declares, "All of that is true. I think in this sense, MoSeq can make eggs and pancakes."

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How video game tech, AI, and computer vision help decode animal pain and behavior

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Top neuroscience labs are adapting new and unexpected tools to gain a deeper understanding of how mice, and ultimately humans, react to different drug treatments.

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This study monitored the neuronal activity and synaptic function of dogs, to investigate the causal relationship of Shank3 mutations and its impact on social behaviour.  Shank3 mutations are highly correlated with Austism Spectrum Disorder. This study believed that the absence of Shank3 in dogs leads to behavioural abnormalities that could be applied to humans with behavioural impairments.

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Smaller PSD of the excitatory synapse in Shank3 mutant dogs. A) Electron microscope images of excitatory synapses in layer 2/3 of PFC. White arrows indicate postsynaptic densities (PSD). B) PSDs are shorter in Shank3 mutants compared with WT controls. C) PSDs are thinner in Shank3 mutants compared with WT controls D Increased density of presynaptic vesicles at the excitatory synapses in mutant dog. Credit: Molecular Autism (2024). DOI: 10.1186/s13229-024-00587-4

Researchers led by Prof. Zhang Yongqing from the Institute of Genetics and Developmental Biology (IGDB) of the Chinese Academy of Sciences have established for the first time a brain slice electrophysiology system in an autism-associated canine model and revealed neuronal structural and functional abnormalities in Shank3 mutant dogs.

The study, titled "Impaired synaptic function and hyperexcitability of the pyramidal neurons in the prefrontal cortex of autism-associated Shank3 mutant dogs," was published in Molecular Autism on Jan. 31.

Shank3 mutations are highly correlated with autism spectrum disorders (ASD). In rodents, the absence of Shank3 leads to abnormal behaviors associated with ASD, including social interaction deficits and repetitive stereotyped behaviors. Synaptic dysfunction and dendritic spine reduction in specific brain regions due to Shank3 deficiency are thought to be the neural basis leading to behavioral impairments.

Given the significant differences in brain structure and social behavior between rodents and humans, such as human interactions involving complex social cognition and understanding while rodents rely primarily on olfaction for communication, there is a challenge in translating findings from rodent models to human patients.

Dogs, which co-evolved with humans over a long history and possess complex interspecies emotional and social processing capabilities, serve as an effective animal model for studying human social behavior and mental disorders. Therefore, detecting changes in neuronal activity and synaptic function in Shank3 mutant dogs is critical to understanding the causal relationship between Shank3 mutations and abnormal social behaviors.

The researchers used Shank3 mutant dogs as a model animal to study the electrophysiological function and morphological characteristics of neurons in the prefrontal cortex, a brain region highly involved in social cognitive behaviors. The results showed that pyramidal neurons in the prefrontal cortex of mutant dogs exhibited increased excitability and decreased excitatory synaptic transmission compared to wild-type dogs.

In addition, reduced dendritic complexity, a lower dendritic spine density, and smaller postsynaptic density structures were also found in Shank3 mutant dogs. These phenotypes suggest that heterozygous Shank3 mutations are sufficient to induce morphological and functional abnormalities in cortical pyramidal neurons, which may contribute to abnormal social behaviors in mutant dogs.

This study demonstrates the feasibility of using canine brain slices to explore neural circuits and mechanisms of ASD.

More information: Feipeng Zhu et al, Impaired synaptic function and hyperexcitability of the pyramidal neurons in the prefrontal cortex of autism-associated Shank3 mutant dogs, Molecular Autism (2024). DOI: 10.1186/s13229-024-00587-4

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Neuronal abnormalities in autism-associated canine model carry Shank3 mutations

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Researchers led by Prof. Zhang Yongqing from the Institute of Genetics and Developmental Biology (IGDB) of the Chinese Academy of Sciences have established for the first time a brain slice electrophysiology system in an autism-associated canine model and revealed neuronal structural and functional abnormalities in Shank3 mutant dogs.

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Are we inching closer to a treatment for Alzheimer's?

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Are we inching closer to a treatment for Alzheimer's?

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The article discusses the various stumbling blocks and recent developments in the search for a treatment for Alzheimer's including a recent study considering the role of "cold shock" proteins in helping protect and repair the brain. There is one small reference to that research showing promise "in mice at least".

Although a small win is that the research paper includes a photograph of mice alongside the abstract which makes it more obvious :/

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At the end of November, thousands of researchers from around the world will descend on San Francisco for the annual Clinical Trials on Alzheimer's Disease meeting. The conference is a mainstay of the dementia research calendar, the place where the latest progress - and all too often, setbacks - in the quest for Alzheimer's treatments are made public for the first time.

This year's meeting is poised to be a landmark event. After more than a century of research into Alzheimer's, scientists expect to hear details of the first treatment that can unambiguously alter the course of the disease. Until now, nothing has reversed, halted or even slowed the grim deterioration of patients' brains. Given that dementia and Alzheimer's are the No 1 killer in the UK, and the seventh largest killer worldwide, there is talk of a historic moment.

The optimism comes from a press statement released in September from Eisai, a Japanese pharmaceutical firm, and Biogen, a US biotech. It gave top-line results from a major clinical trial of an antibody treatment, lecanemab, given to nearly 2,000 people with early Alzheimer's disease. The therapy slowed cognitive decline, the statement said, raising hopes that a drug might finally apply the brakes to Alzheimer's and provide " a clinically meaningful impact on cognition and function ".

The announcement was greeted, broadly, with delight and relief from researchers who have endured failure after failure in the long search for Alzheimer's drugs. But even the most enthusiastic conceded that significant questions remained. With only a press release to go on, it was hard to be sure the claims stood up. The answer will come on 29 November when researchers leading the trial, named Clarity AD, present their results at the San Francisco meeting.

'If you can slow the decline, even a small amount, you will really start to see an impact at the economic and medical level.' Illustration: Thomas Hedger at Grand Matter/The Guardian

Lecanemab has already sparked debate. Antibody drugs are so costly they are beyond the means of many countries. Lecanemab itself is not easy to administer, unlike pills and capsules: patients are required to attend clinic for an intravenous infusion twice a month. And the side-effects call for extensive monitoring: patients on the trial had regular scans for brain swelling and haemorrhages, a service many hospitals cannot provide at scale.

More importantly, lecanemab might not work very well. From the data released so far, it is unclear what difference it could make to the devastating burden inflicted by Alzheimer's. Some doctors warn that the benefits of the drug seem so small, patients may not even notice. But others counter that any effect on Alzheimer's deserves celebration: it proves the disease can be beaten, or at least slowed down. It's a start, a concrete foundation to build on.

"Dementia is a global economic disaster as people are institutionalised while their disease progresses at huge cost to society and healthcare systems," says Prof Giovanna Mallucci, former centre director of the UK Dementia Research Institute at the University of Cambridge, now principal investigator at Altos Labs. "If you can slow the decline, even a small amount, you will really start to see an impact at the economic and medical level."

'I feel like we might be able to offer something decent to patients within the next few years' ... Prof Bart De Strooper. Photograph: Ine Dehandschutter/Ine Dehandschutter/VIB

Researchers liken the situation to the HIV crisis in the 1980s. The first anti-HIV drug was far from ideal, but it paved the way for the highly effective therapies used today. "When you have that first breakthrough, it's like the hole in the dyke that leads to a bigger hole," says Prof Bart De Strooper, director of the UK Dementia Research Institute at University College London. "There is much more belief now that we can find something. As a doctor, I feel like we might be able to offer something decent to patients within the next few years."

"This is not a cure by any stretch of the imagination, but if it does slow cognitive decline, it means that for the first time we are modifying the disease," says Dr Richard Oakley, head of research at the Alzheimer's Society. "We need to understand the real-world clinical benefit, but I've spoken to people and where there's never been excitement, always hesitation, this does look like the real deal. We need to see the data, but everyone is now saying this is the beginning of disease-modifying treatments."

Alzheimer's accounts for more than 60% of the 55 million cases of dementia worldwide. The condition costs the UK £25bn a year, a figure that is on course to nearly double to £47bn by 2050. The most common early signs are memory problems, but as the disease progresses, people can find themselves lost in familiar places, having trouble with decisions, struggling with simple tasks, experiencing mood swings and changes in personality. It is a terminal condition: typically, people die within eight years of an Alzheimer's diagnosis.

If we think about Alzheimer's in old age, I think most people have mixed forms of dementia

The cognitive decline in Alzheimer's arises from the relentless destruction of neurons, the cells that ferry information around the brain. The effect goes far beyond normal age-related brain shrinkage: on death, a patient's brain can weigh 140g less than before the disease took hold - a reduction of more than 10%.

Exactly what kills the brain cells is still up for debate. In some families blighted by early onset Alzheimer's, scientists have found mutations that cause abnormal clumps, or plaques, of a brain protein called amyloid beta to build up between neurons. Above a certain tipping point, these plaques seem to aid the formation of harmful tangles of another brain protein called tau. These accumulate inside the neurons themselves. More tangles tend to mean greater cognitive decline.

But inherited forms of Alzheimer's are rare. In most patients, the decline is likely to be driven by a messy mix of processes, which fuel one another. Amyloid and tau are still in the frame, but other toxic proteins, chronic inflammation, vascular problems, cellular health, and faulty disposal of waste from the brain may all contribute. "If we think about Alzheimer's in old age, I don't think most of these people have pure Alzheimer's," says De Strooper. "I think they have mixed forms of dementia. It's not always clear what's really driving the disease."

Efforts to develop Alzheimer's drugs have focused overwhelmingly on amyloid. Some aim to block enzymes involved in the production of abnormal amyloid, while others, such as lecanemab, are antibodies designed to clear it from the brain. Between 2007 and 2019, more than a dozen final-stage, or "phase 3", trials of amyloid-targeting drugs reported results. None slowed cognitive decline; some even made it worse.

A computer-generated image of amyloid plaques - misfolded proteins that aggregate between neurons. Photograph: Artur Plawgo/Getty Images/iStockphoto

The failures split the research community. Some threw out the entire amyloid hypothesis. Others concluded that even if it was valid, amyloid wasn't the best protein to target. Further concerns surrounded the trials themselves: many enrolled patients who already had Alzheimer's symptoms. For them, removing amyloid may be too little, too late: snuffing out the match once the fire is raging. The problem is compounded by the insidious early phase of the disease, which destroys neurons without people noticing. "Your brain is so plastic that it can cope with a lot of damage before it starts to show symptoms," says De Strooper.

In June last year, the US Food and Drug Administration gave the green light to the first new drug for Alzheimer's in nearly 20 years. Biogen's Aduhelm (aducanumab) became the first approved therapy to target amyloid, but the decision provoked a furore. An independent FDA committee advised against approval because Biogen's trial data failed to show clear benefit.

But the FDA granted "accelerated approval" because it cleared amyloid plaques from patient's brains, and therefore might slow the progression of Alzheimer's if taken early enough, and for long enough. Several scientists resigned from the committee in protest, including Prof Aaron Kesselheim at Harvard Medical School, who told the regulator that its ruling was " probably the worst drug approval decision in recent US history ".

The FDA will rule on lecanemab in January 2023, with decisions in the UK and Europe to follow. While press-released data from the lecanemab trial suggests the drug slowed cognitive decline, the effect was small. After 18 months, cognition declined 27% less in those who took the drug compared with those on a placebo. On a common dementia rating scale, which scores people from 0 to 18 on memory, problem-solving and other tasks, those on lecanemab performed only 0.45 points better. The result is statistically significant, but it may not mean much for individual patients.

"The effect they've reported to date is very small. It's not large enough to be clinically important," says Prof Victor Henderson, director of the Alzheimer's Disease Research Center at Stanford University. He warns that there is a subjective element to the dementia ratings that could matter when the observed benefit is so marginal. "I would be concerned that this could be a drug that has statistical significance without clinical significance and we may need to wait for something better," he says.

One idea gaining ground in Alzheimer's research is that drugs will need to remove amyloid fast to have any hope of showing a clinical benefit. The logic is laid out in a 2022 paper by De Strooper and Eric Karran at AbbVie, a US biopharmaceuticals firm. They argue that it will take time for the effects of amyloid removal to show up in thinking and memory tests. If a drug doesn't push amyloid low enough, or takes years to do it, it probably won't help, they suggest, at least not in the timeframe of most clinical trials.

Despite lecanemab's reportedly small effect, Mallucci sees positives in the results. "What really needs to be trumpeted from this trial [assuming the results hold up] is that you can change the rate of decline of the disease. That half a point is subtle and the individuals might not feel very different, but you can build on it," she says.

It's likely that more research has been done on Covid in the past three years than on dementia in the past century. Photograph: Cultura Creative Ltd/Alamy

Chronic underfunding means patients have already waited too long for progress. Earlier this year, De Strooper searched the US medical database PubMed for dementia. He found 250,000 studies. He then searched for cancer and found 4.7m. Next, he searched for Covid, a disease that didn't exist before 2019, and found 300,000 studies. It's a rough metric, but it suggests that more research has been done on Covid in the past three years than on dementia in the past century.

The comparison with cancer is particularly striking. Decades of substantial funding and research have transformed cancer diagnosis and care. Under NHS England targets, people should wait no more than 28 days from referral to hear whether or not they have cancer. But for dementia, NHS England has only an "ambition" to diagnose two-thirds of patients. No timescale is mentioned.

With cancer, the full suite of diagnostic equipment is brought to bear on patients, from genome sequencing to advanced MRI and PET scanners. People often receive a detailed diagnosis of the cancer they have. Dementia diagnosis and care lag far behind. If Alzheimer's patients can benefit from amyloid-clearing treatments, they will need an early diagnosis and evidence of amyloid in the brain. UK clinics are not close to being able to offer such services. "We could be in the situation in 2025 when we have access to a drug that modifies disease but are unable to give it to those most likely to benefit because we diagnose them too late and unspecifically," says Oakley.

The real hope may lie in entirely different approaches. Antibodies may help some Alzheimer's or pre-Alzheimer's patients, but to have a major effect on the disease, a combination of drugs that hit different biological processes is needed. "I suspect antibodies will have a place for a small number of carefully selected patients, but we need multiple approaches," says Mallucci. "This isn't a feasible way forward for dementia treatment on a global scale. It's not feasible economically or logistically."

One idea is to administer vaccines that prompt the patient's immune system to churn out antibodies to clear problematic amyloid and tau. De Strooper believes drugs that block key enzymes needed for the production of harmful amyloid are worth another look. Mallucci favours drugs that make the ageing brain more resilient, by protecting and reinvigorating brain cells. There are many potential approaches, including boosting the brain's ability to clear toxic proteins and targeting inflammation. She has pioneered work on increasing the fitness of diseased brain cells, the ability to make new proteins, and on the "cold-shock" protein RBM3, which mammals release in hibernation and hypothermia. Both these approaches help to regenerate synapses, the connections between neurons, and - in mice, at least - help to protect against dementia by boosting memory and preventing brain cell death.

Another line of attack is to boost a compound called BDNF, which might also reinvigorate cells and help them build new connections. A new clinical trial at the University of California, San Diego, is about to test whether a BDNF-boosting gene therapy can help patients with early Alzheimer's.

And this is what the field needs, says Oakley: more funding, more approaches, more trials. "We are beginning to see a future where we can make dementia a chronic condition, one you live with and die with but don't die from," he says. "We've seen it work in every other major condition that research has tackled, and we will see it in dementia. This first generation of amyloid-clearing drugs is only the beginning."

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'This looks like the real deal': are we inching closer to a treatment for Alzheimer's?

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After years of setbacks, dementia researchers are getting excited about a new antibody drug called lecanemab. No one expects it to stop cognitive decline, but even slowing it would be a breakthrough

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Gut microbes may play role in social anxiety disorder

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Gut microbes may play role in social anxiety disorder

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It is made clear that the study involved mice.

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While some people might relish the prospect of a new year party, for others socialising can trigger feelings of fear, anxiety and distress. Now researchers say microbes in the gut may play a role in causing social anxiety disorder, opening up fresh possibilities for therapies.

Scientists have previously found the gut microbiome - the collection of bacteria and other organisms that live in the gastrointestinal system - differs for people who have social anxiety disorder (SAD) compared with healthy individuals, while a growing body of research has revealed that microbes in the gut can influence the brain - and vice versa.

Now researchers have found that when microbes from the guts of people with SAD are transplanted into mice, the animals have an increased response to social fear.

The findings build on previous work showing similar results for conditions ranging from depression to irritable bowel syndrome.

Prof John Cryan, a co-author of the research from University College Cork, said that while it was known that genetics, the environment and other factors could also play a role in disorders including SAD, the new work highlighted the importance of our gut flora.

"The main point is we need to look after our microbes, especially throughout development and even in adulthood, to keep the social brain working appropriately," he said.

Writing in the Proceedings of the National Academy of Sciences, Cryan and colleagues report how they took faecal samples from six healthy people and six people with SAD, with DNA analyses confirming that the gut microbiome differed considerably between the two groups.

The team transferred each sample into six laboratory mice, giving a total of 72 creatures, all of whom had previously been given antibiotics to kill off their natural gut microbes.

The mice were subsequently presented with a series of tests to explore various aspects of their behaviour. To investigate social fear, the team gave the mice small electric shocks when they approached a new mouse, and then observed how the animals behaved around new mice when the shocks were no longer applied.

The results revealed that the mice who had received gut microbes from people with SAD had different levels of three bacterial species in their faeces than those who had received gut microbes from healthy people.

The team add that while behaviour of the mice did not differ for most of the experiments investigating anxiety and social behaviour, they did behave differently after the social fear experiment. While mice with gut microbes from healthy people quickly regained their curiosity towards strangers in the days that followed, those with microbes from people with SAD continued to be fearful of approaching other mice.

"They never fully recovered to be able to be social again," said Cryan.

Further analysis suggested levels of certain hormones and aspects of the immune system also differed between the mice.

"Both oxytocin, a key hormone involved in bonding, and the immune system have previously been implicated in social behaviour, therefore it was good to see that changes in these occurred in animals that received the SAD microbiota," said Cryan.

The team say the results suggest the gut microbiome can play a causal role in heightened social fear responses in social anxiety disorder, while the study also offers new avenues when it comes to developing therapeutics for people with SAD.

Cryan said that could include diets designed to alter the microbiome.

"Increasing the amount of fibres and fermented foods in the diet may have beneficial effects," he said. "And that's something that we're quite interested in exploring."

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Gut microbes may play role in social anxiety disorder, say researchers

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Study that involved transplanting people's microbes into mice may show way to possible therapies, say scientists

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Optimistic: One of many articles accessed on Science Daily that DID mention the use of animals in the original experiments :D

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Optimistic: One of many articles accessed on Science Daily that DID mention the use of animals in the original experiments :D

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https://www.sciencedaily.com/releases/2024/02/240220144401.htm

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Blocking key protein may halt progression of Alzheimer’s disease

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Researchers have found that inhibiting a key protein can stop the destruction of synapses and dendritic spines commonly seen in Alzheimer’s disease.

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Pigs instead of mice. The article briefly mentions in the middle that the study was done on pigs and creates the impression it was done on humans, including the attached photo

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Vibrating pill may give dieters a feeling of fullness, study suggests

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Research carried out on pigs showed they ate almost 40% less food after ingesting the capsule

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Loneliness hurts not just men’s mental health — it may hurt their bones, too: study

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Loneliness hurts not just men’s mental health — it may hurt their bones, too: study

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Mice are mentioned in the article, but not until towards the end

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Loneliness is not just bad for men's mental health - it may be bad for their bones, too, according to a new study.

And while social isolation may have a negative impact on the bone health of men, this is not true of women, the researchers found.

Dr. Rebecca Mountain, of Maine Health Institute for Research in Scarborough, Maine, was lead researcher on the study, as multiple outlets reported.

The study was presented on Sunday at ENDO 2023, the Endocrine Society's annual meeting, in Chicago, Illinois.

"Social isolation is a potent form of psychosocial stress," said Dr. Mountain in a statement, "and is a growing public health concern, particularly among older adults."

She also said, "Even prior to the onset of the COVID-19 pandemic, which has significantly increased the prevalence of isolation and loneliness, researchers have been concerned about a rising 'epidemic of loneliness,'" as SWNS reported.

Social isolation, she also said, is associated with an increased risk for many health conditions, including mental disorders, as well as higher overall rates of illness and death.

"Previous clinical research," she said, "has demonstrated that psychosocial stressors, and subsequent mental health disorders, are major risk factors for osteoporosis and fracture, which disproportionally affect older adults."

A new study found that loneliness can be bad for men's mental health and bone health. Shutterstock

She added that the impacts of social isolation on "bone, however, have not been thoroughly investigated."

In the study, researchers exposed adult mice to social isolation - meaning one mouse per cage - or grouped housing, with four mice per cage - for four weeks.

The scientists found that social isolation caused significant reductions in bone quality, including reduced bone mineral density, in the male mice - but not the female mice.

The article's abstract indicated that "isolated male mice had signs of reduced bone remodeling represented by reduced osteoblast numbers [cells that form new bones], osteoblast-related gene expression and osteoclast-related gene expression. However, isolated females had increased bone resorption-related gene expression, without any change in bone mass."

More study is needed on the topic

Dr. Mountain said, "Overall, our data suggest that social isolation has a dramatic negative effect on bone in male mice, but it may operate through different mechanisms or in a different time frame in female mice."

She added, "Future research is needed to understand how these findings translate to human populations."

She also said, "Our work provides critical insight into the effects of isolation on bone and has key clinical implications as we grapple with the long-term health impacts of the rise in social isolation related to the COVID-19 pandemic."

According to the study's lead researcher, loneliness is a "form of psychosocial stress." Shutterstock

The Endocrine Society is a global community of physicians and scientists "dedicated to accelerating scientific breakthroughs and improving patient health and well-being," the group says on its website.

Maine Health Institute for Research, for its part, supports and encourages a "broad spectrum of research," the group says on its site, "ranging from basic laboratory-based research through translational research, which works to apply basic discoveries to medical problems, to clinical research, which studies the direct application of new drugs, devices and treatment protocols to patients, to health services research which seeks to use research methods to help improve and evaluate health care delivery programs and new technologies."

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Loneliness hurts not just men's mental health - it may hurt their bones, too: study

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Social isolation, according to an expert, is associated with an increased risk for many health conditions, including mental disorders, as well as higher overall rates of illness and death.

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Interesting as this talks about types of neurons for navigation and creating AI algorithms.

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An artificial intelligence can interpret a mouse's brain activity to tell scientists where the animal is located and the direction it is looking

A micrograph of a section through a mouse's brain highlighting neural pathways (green)

MARK AND MARY STEVENS NEUROIMAGING AND INFORMATICS INSTITUTE/SCIENCE PHOTO LIBRARY

Analysing a mouse's brain activity tells scientists where the animal is located and the exact direction it is looking. With further research, the findings could one day help robots navigate autonomously.

Mammalian brains use two main types of neurons for navigation: "head direction cells" show where an animal is facing and "grid cells" help provide a two-dimensional brain map of where it is located.

To learn more about the firing of these neurons, Vasileios Maroulas at the University of Tennessee, Knoxville, and his colleagues - together with the US Army Research Laboratory - analysed data from a previous study.

In this experiment, probes were inserted into several mice's brains. Data on their neural firing patterns were then paired with video footage showing their locations and head positions as they moved around an open environment.

From this, Maroulas and his colleagues developed an artificial intelligence algorithm that can use neural activity to work out where a mouse is looking and where it is located.

In effect, it is like the drop pin and directional arrow on a smartphone's map app, except instead of connecting to a GPS satellite, scientists analyse a subject's brain signals.

"This method allows us to not be dependent on a preloaded map or updating the GPS coordinates based on, say, satellite data," says Maroulas. "In some sense, the algorithm 'thinks' and recognises space as a mammalian brain would."

The AI could eventually enable intelligent systems to navigate autonomously, he says. "In other words, we take advantage of how the mammalian brain processes data and incorporate it in the architecture of the algorithm."

Adam Hines at the Queensland University of Technology in Australia says the smartphone app analogy is a helpful one. "You have positional information (the drop pin) aligned with direction (blue arrow), and during navigation the two are constantly updating as you move. Grid cells are like the GPS and heading cells are like a compass."

Topics:

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AI can tell where a mouse is by reading its brain activity

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An artificial intelligence can interpret a mouse's brain activity to tell scientists where the animal is located and the direction it is looking

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Wildfire Smoke Altered Brain Structures Related to Memory in Mice

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Wildfire Smoke Altered Brain Structures Related to Memory in Mice

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Exposure to smoke led to neurodegenerative changes for mice in the hippocampus (subcortical structure which is particularly crucial in memory and learning). The study authors postulate that this has implications for future rates of dementia and Parkinson's disease in humans, in a world more prone to wildfires due to anthropogenic climate change.

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Wildfire Smoke Altered Brain Structures Related to Memory in Mice

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Inhalation of particulate matter present in wildfire smoke may pose risk to the aging brain.

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A neural circuit for male sexual behavior and reward

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A neural circuit for male sexual behavior and reward

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https://www.cell.com/cell/fulltext/S0092-8674(23)00798-5?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0092867423007985%3Fshowall%3Dtrue

Title is ambiguous and has no mention of mice in the summary (in place of an abstract) which could lead to some amusement.

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Environmental enrichment promotes adaptive responding during tests of behavioral regulation in male heterogeneous stock rats 

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Environmental enrichment promotes adaptive responding during tests of behavioral regulation in male heterogeneous stock rats 

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https://pubmed.ncbi.nlm.nih.gov/38378969/

Is clear from the start that rats are involved in the study, and is mentioned already in the abstract.

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Affiliations

¹ Clinical and Research Institute on Addictions, University at Buffalo, Buffalo, NY, USA.

² Department of Pharmacology and Toxicology, University at Buffalo, Buffalo, NY, USA.

³ Department of Psychology, University at Buffalo, Buffalo, NY, 14260, USA.

⁴ Department of Psychiatry, University of California San Diego, La Jolla, CA, USA.

⁵ Department of Internal Medicine, Molecular Medicine, Center on Diabetes, Obesity and Metabolism, Wake Forest School of Medicine, Winston-Salem, NC, USA.

⁶ Department of Psychology, California State University, Bakersfield, CA, USA.

⁷ Institute for Genomic Medicine, University of California San Diego, La Jolla, CA, USA.

⁸ Department of Behavioral Neuroscience, Oregon Health & Science University, Portland, OR, USA.

⁹ Department of Psychiatry, Oregon Health & Science University, Portland, OR, USA.

¹⁰ Oregon Institute for Occupational Health Sciences, Oregon Health & Science University, Portland, OR, USA.

¹¹ Department of Psychology, University at Buffalo, Buffalo, NY, 14260, USA. pmeyer@buffalo.edu.

Free PMC article

Free PMC article

Affiliations

¹ Clinical and Research Institute on Addictions, University at Buffalo, Buffalo, NY, USA.

² Department of Pharmacology and Toxicology, University at Buffalo, Buffalo, NY, USA.

³ Department of Psychology, University at Buffalo, Buffalo, NY, 14260, USA.

⁴ Department of Psychiatry, University of California San Diego, La Jolla, CA, USA.

⁵ Department of Internal Medicine, Molecular Medicine, Center on Diabetes, Obesity and Metabolism, Wake Forest School of Medicine, Winston-Salem, NC, USA.

⁶ Department of Psychology, California State University, Bakersfield, CA, USA.

⁷ Institute for Genomic Medicine, University of California San Diego, La Jolla, CA, USA.

⁸ Department of Behavioral Neuroscience, Oregon Health & Science University, Portland, OR, USA.

⁹ Department of Psychiatry, Oregon Health & Science University, Portland, OR, USA.

¹⁰ Oregon Institute for Occupational Health Sciences, Oregon Health & Science University, Portland, OR, USA.

¹¹ Department of Psychology, University at Buffalo, Buffalo, NY, 14260, USA. pmeyer@buffalo.edu.

Abstract

Organisms must regulate their behavior flexibly in the face of environmental challenges. Failure can lead to a host of maladaptive behavioral traits associated with a range of neuropsychiatric disorders, including attention deficit hyperactivity disorder, autism, and substance use disorders. This maladaptive dysregulation of behavior is influenced by genetic and environmental factors. For example, environmental enrichment produces beneficial neurobehavioral effects in animal models of such disorders. The present study determined the effects of environmental enrichment on a range of measures related to behavioral regulation using a large cohort of male, outbred heterogeneous stock (HS) rats as subjects. Subjects were reared from late adolescence onwards either in pairs in standard housing with minimal enrichment (n = 200) or in groups of 16 in a highly enriched environment consisting of a large multi-level cage filled with toys, running wheels, and shelters (n = 64). Rats were subjected to a battery of tests, including: (i) locomotor response to novelty, (ii) light reinforcement, (iii) social reinforcement, (iv) reaction time, (v) a patch-depletion foraging test, (vi) Pavlovian conditioned approach, (vii) conditioned reinforcement, and (viii) cocaine conditioned cue preference. Results indicated that rats housed in the enriched environment were able to filter out irrelevant stimuli more effectively and thereby regulate their behavior more efficiently than standard-housing rats. The dramatic impact of environmental enrichment suggests that behavioral studies using standard housing conditions may not generalize to more complex environments that may be more ethologically relevant.

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Conflict of interest statement

The authors declare no competing interests.

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Alemany S, et al. New suggestive genetic loci and biological pathways for attention function in adult attention-deficit/hyperactivity disorder. Am. J. Med. Genet. B Neuropsychiatr. Genet. 2015;168:459-470. doi: 10.1002/ajmg.b.32341. - DOI - PubMed

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national center for biotechnology information

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Environmental enrichment promotes adaptive responding during tests of behavioral regulation in male heterogeneous stock rats - PubMed

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Organisms must regulate their behavior flexibly in the face of environmental challenges. Failure can lead to a host of maladaptive behavioral traits associated with a range of neuropsychiatric disorders, including attention deficit hyperactivity disorder, autism, and substance use disorders. This ma ...

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Tickling rats to learn about which brain regions involved in play 

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Tickling rats to learn about which brain regions involved in play 

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Playful behaviour has been observed in many species. Researchers found both tickling and playing lit up the PAG region (the midbrain region called periaqueductal gray) in rodents. The article states play and tickling involve some of the same brain circuitry. The article suggests since playful behaviour is exhibited in both animals and humans, it may be an evolutionary adaptation. The article also talks about the importance of play.

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Scientists tickle rats to learn about brain activity during play | CNN

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Researchers played with and tickled rats in a study, identifying a part of the brain that's active both when the rodents are playing and when they're tickled.

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BBC News - "How Brain Cells Die in Alzheimer's"

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BBC News - "How Brain Cells Die in Alzheimer's"

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The article does mention mice, but not until the very end of the article

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Scientists discover how brain cells die in Alzheimer's

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The findings, which had been a mystery for decades, give new ideas for treating the disease.

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Importance of accounting for gender differences in research on how stress affects brain cells

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Importance of accounting for gender differences in research on how stress affects brain cells

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https://scitechdaily.com/is-stress-gender-blind-new-research-says-no-and-the-implications-are-huge/

This study looked into the effects of stress on different brain cell types, in both male and female mice.

The fact that the study is based on mice is emphasised in the summary, start of the article, end of the article, and in the citation.

The middle of the article (which is a large bulk) summarises the study's findings. It is generally written as brain cell research, and differing stress responses by brain cells in males and females. There is little-no reference to animal/that the research was done on mice in this section.

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The article is about a research study on mice investigating how body sensations can influence emotions in the brain. The study artificially increased heartbeats in mice to a level they would experience in stressful situations. With the increased heartbeat, the mice displayed behaviour associated with anxiety and showed activity in the posterior insula, which has a lot of interoceptive circuitry connections. The article suggests the body may be able to influence emotions in the brain. The article is very clear it was based on mice and even includes pictures of mice.

Personally, I'm not comfortable with animal research, but taking a different viewpoint it is probably quite difficult to get ethical approval to conduct a similar experiment on humans.

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Questions or comments on this article? E-mail us at feedback@sciencenews.org | Reprints FAQ

Editor's Note:

This story was updated March 21, 2023, to correct Wen Chen's title.

A version of this article appears in the April 8, 2023 issue of Science News.

Bethany was previously the staff writer at Science News for Students. She has a Ph.D. in physiology and pharmacology from Wake Forest University School of Medicine.

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In mice, anxiety isn't all in the head. It can start in the heart

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Scientists used optogenetics to raise the heartbeat of a mouse, making it anxious. The finding could offer a new angle for studying anxiety disorders.

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Reused Cooking Oil Ups Risk Of Metastases In Breast Cancer Patients

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Reused Cooking Oil Ups Risk Of Metastases In Breast Cancer Patients

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Totally misleading title and mice are not mentioned until the methods

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Reused Cooking Oil Ups Risk Of Metastases In Breast Cancer Patients

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Using cooking oil multiple times and at high heat increases its likelihood to cause cancer. These oils have properties that trigger tumor cell proliferation, metastases, and lipid metabolism changes.

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Animal Research that Respects Animal Rights: Extending Requirements for Research with Humans to Animals

by Angela K. Martin

https://philarchive.org/archive/MARART-26