#micestudy — Public Fediverse posts
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DATE: September 5, 2026 at 08:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Scientists map the brain pathway that links social isolation to increased alcohol consumption
A recent study in mice suggests that social isolation drives increased alcohol consumption by strengthening a specific neural pathway in the brain, though this effect appears to operate differently in males and females. The findings provide a biological mechanism for how negative social environments can heighten the risk of alcohol misuse. The research was published in Nature Neuroscience.
The basolateral amygdala is an almond-shaped structure deep in the brain that processes emotions and stress. The medial prefrontal cortex is a region at the front of the brain responsible for decision-making, executive control, and evaluating rewards. Researchers know that social isolation is a major risk factor for heavy drinking, and past work laid the foundation for understanding how the brain handles these specific stressors.
For example, a 2017 study showed that signals flowing from the amygdala to the prefrontal cortex guide decisions when animals face competing reward and threat cues. Building on this, a 2020 study found that stress physically strengthens the pathway connecting the amygdala to the prefrontal cortex, increasing anxiety-like behaviors. This progression led researchers to explore whether this specific communication highway, the pathway from the basolateral amygdala to the medial prefrontal cortex, drives isolation-induced alcohol misuse and whether the effects differ by sex.
The new research was led by Reesha R. Patel, an assistant professor at Northwestern University Feinberg School of Medicine, and Kay M. Tye, a professor at the Salk Institute for Biological Studies. The scientists aimed to map exactly how social isolation alters this brain circuit to influence drinking habits.
“Social isolation is increasingly recognized as an important risk factor for problematic alcohol use, but we know surprisingly little about how social experience actually changes the brain in ways that can influence drinking,” Patel told PsyPost. “We wanted to move beyond the association between isolation and alcohol use and identify the specific neural circuit changes that could contribute to this vulnerability.”
The researchers began by observing 14 male and 11 female mice in a choice setup, where the animals had access to both water and a 15% alcohol solution. They tracked the animals’ drinking while group-housed and then over 11 days of social isolation.
The isolation produced opposite behavioral effects depending on the sex of the mouse. Isolated males progressively increased their alcohol intake, while isolated females drank less alcohol. The researchers also noted that an animal’s social rank influenced its habits, as subordinate mice of both sexes tended to drink more alcohol than dominant mice even before being isolated.
“One other interesting finding was that social rank also predicted how much the mice drank even before isolation,” Patel said. “That suggests that alcohol drinking is shaped not just by whether an animal is socially isolated, but also by its social experience more broadly. We’re interested in understanding how different aspects of the social environment influence the brain and drinking behavior.”
Next, the team examined the brain cells connecting the basolateral amygdala to the medial prefrontal cortex. They used a technique called patch-clamp electrophysiology, which uses tiny glass electrodes to measure the electrical activity of individual neurons. The electrical excitability of these specific neurons closely mirrored the drinking behaviors.
In males, social isolation increased the excitability of these connecting neurons, making them more likely to fire. In females, isolation decreased this excitability. Because only males reliably escalated their drinking during isolation, the researchers focused the rest of their experiments on male mice to isolate the biological mechanisms driving increased alcohol use.
To see how this circuit behaves in real time, the team used cellular-resolution calcium imaging. They implanted miniature microscopes to track the activity of specific neurons while the male mice participated in a cued drinking task, where a light signaled the availability of alcohol or water. The neurons strongly encoded and predicted alcohol drinking.
Higher electrical activity in this specific brain pathway was linked to a higher frequency of alcohol drinking bouts. The pathway did not show the same predictive relationship for water consumption. The scientists then tested whether activating this pathway could directly influence behavior.
They used optogenetics, a technique where neurons are genetically modified to respond to light. By shining a laser through an implanted fiber, they could manually turn on the pathway from the basolateral amygdala to the medial prefrontal cortex whenever a mouse licked the drinking spout. Activating the circuit specifically increased alcohol intake, prompting the mice to engage in longer drinking bouts and take more licks per bout.
This light stimulation did not affect how much water or sugar water the mice drank. To understand how this signal changes the brain’s broader evaluation of rewards, the team tracked the activity of downstream neurons in the medial prefrontal cortex. During social isolation, the prefrontal cortex became much more responsive to alcohol but less responsive to natural rewards like sugar water.
“One of many actually surprising findings was that isolation changed how the prefrontal cortex represented different rewards,” Patel noted. “That raises the possibility that social experience can alter the relative value the brain assigns to different rewards.”
When the researchers artificially stimulated the pathway in group-housed mice, the prefrontal cortex reacted exactly as it did in isolated mice, showing heightened responses to alcohol and dampened responses to sugar. Finally, the researchers used optogenetics to inhibit, or silence, the pathway in socially isolated male mice. Turning off this circuit reduced the number of alcohol drinking bouts the isolated mice initiated, without affecting their water consumption.
This indicates that this specific neural pathway actively drives the escalation in alcohol use following social isolation. “Social isolation does not simply make animals drink more — it changes how one specific amygdala-to-prefrontal pathway represents alcohol relative to natural rewards,” said Jun Wang, a professor in the Department of Neuroscience and Experimental Therapeutics at Texas A& M University Health Science Center, who was not involved in the research.
“That coupling is the striking part,” Wang told PsyPost. “It offers a circuit-level account of how a social risk factor gets converted into a change in what the brain treats as worth pursuing, rather than just a change in how much an animal consumes.”
“I think the biggest takeaway is that our social experiences can have very real effects on the brain,” Patel said. “Social isolation didn’t just change how much the mice drank, it changed the activity of a specific brain circuit that helped drive that increase in alcohol use. To me, that really emphasizes that our social environment is an important part of understanding vulnerability to things like excessive drinking.”
“The broader significance is that social isolation may not simply be a circumstance that accompanies increased alcohol use—it can produce biological changes in the brain that actively contribute to drinking behavior,” she explained. “Understanding those mechanisms could ultimately help explain why social isolation increases vulnerability to problematic alcohol use in some individuals and may point toward new ways of identifying or reducing that vulnerability.”
Wang noted that the study’s strength lies in pinning the behavioral change directly to this specific brain projection and demonstrating that it is both necessary and sufficient. “The sex difference is the most interesting extension,” he added. “Two opposite behavioral outcomes, one consistent circuit signature.”
He also pointed out that the social-rank findings are a “genuinely new addition, and a reminder that the relevant social variable is not only isolation.”
The findings are in line with research covered by PsyPost earlier this year, which found that social isolation increased alcohol intake and altered reward processing in the brain. However, that previous study examined the long-term effects of adolescent isolation in rats, whereas the new research focused on concurrent adult isolation in mice.
As with all research, there are some caveats to consider. Wang expressed reasonably high confidence in the findings for male mice due to the convergence of multiple methods, noting that “together they are difficult to explain away.” However, he pointed out that group sizes were typical for the field but relatively small, and that the experimental drinking model represents escalated voluntary intake, not addiction.
“Nothing here tests compulsive drinking, drinking despite negative consequences, or withdrawal, so ‘isolation causes alcohol use disorder’ is a step beyond the data,” Wang explained. Patel echoed this sentiment, emphasizing that the study relies on animal models, and human social dynamics involve far more complex psychological factors.
“I would be cautious about interpreting the study as showing that loneliness inevitably causes people to drink more,” Patel cautioned. “We experimentally manipulated social isolation in mice, which is not the same thing as the subjective experience of loneliness in humans, and we actually observed very different responses in males and females. What the study provides is evidence that social experience can directly alter neural circuits controlling alcohol-related behavior.”
The researchers and Wang both highlight the unresolved questions regarding female mice, as the exact biological reasons why female mice reduced their drinking during isolation remain unconfirmed. Wang noted that the female mice drank more at baseline, adding that “‘Males escalate, females do not’ is a statement about one mouse strain over about two weeks of isolation.” Because the mechanistic experiments were done only in males, the circuit’s exact role in females remains unknown.
The researchers note that females showed higher baseline excitability in this brain pathway compared to males, suggesting that sex-specific hormonal or physiological mechanisms dictate how these neurons adapt to stress. “One major question is why the same social experience produces such different adaptations across individuals and between males and females,” Patel said.
Wang agreed, emphasizing the need to causally test the pathway in females to see if its downstream consequences differ. He also suggested investigating which prefrontal output pathways actually carry the effect on drinking, and whether the behavioral and brain changes are reversible.
“Does returning animals to group housing normalize both the excitability change and the drinking, and is there a duration of isolation past which it does not?” Wang asked. “That question matters most for the human parallel.”
“We also want to understand the molecular mechanisms that make these circuits sensitive to social experience and whether the resulting neural changes can be reversed,” Patel added. “Ultimately, the broader goal is to understand why adverse social environments increase vulnerability to psychiatric and substance-use disorders in some individuals but not others.”
The study, “Social isolation recruits amygdala–medial prefrontal cortex projections to escalate alcohol drinking in male mice,” was authored by Reesha R. Patel, Kelly N. Kim, Makenzie Patarino, Rachelle Pamintuan, Felix H. Taschbach, Hao Li, Bitna Joo, Anna Pallé, Xianru Yu, Christopher R. Lee, Aniek van Hoek, Jesse White, Rogelio Castro, Christian Cazares, Raymundo L. Miranda, Caroline Jia, Jeremy Delahanty, Kanha Batra, Laurel R. Keyes, Avraham Libster, Romy Wichmann, Talmo D. Pereira, Marcus K. Benna, and Kay M. Tye.
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #SocialIsolation #AlcoholUse #AmygdalaToPrefrontalCircuit #Neuroscience #SexDifferences #MiceStudy #NeuralPathways #NatureNeuroscience #RewardProcessing #Optogenetics
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DATE: September 4, 2026 at 08:29AM
SOURCE: SCIENCE DAILY MIND-BRAIN FEEDTITLE: Stanford scientists discover a seafood that can reverse signs of aging
URL: https://www.sciencedaily.com/releases/2026/09/260902234518.htm
A substance found in edible sea squirts appeared to reverse several signs of aging in older mice. Plasmalogen supplements improved memory and learning, strengthened connections between brain cells, reduced inflammation, and even helped the mice grow thicker, darker hair. Researchers believe the compounds may encourage brain regeneration and protect aging synapses.
URL: https://www.sciencedaily.com/releases/2026/09/260902234518.htm
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #Stanford #SeafoodScience #AgingResearch #Plasmalogen #MemoryImprovement #BrainHealth #SynapseProtection #MiceStudy #SeafoodBenefits #AgeReversal
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DATE: September 3, 2026 at 06:29AM
SOURCE: SCIENCE DAILY MIND-BRAIN FEEDTITLE: One immune switch may help drive aging across the body
URL: https://www.sciencedaily.com/releases/2026/09/260901010717.htm
Aging may be partly fueled by immune cells losing their ability to clear away damaged, inflammation-promoting cells. Blocking a single receptor restored that cleanup process in mice, reducing inflammation and helping their organs, muscles, and memory remain remarkably youthful.
URL: https://www.sciencedaily.com/releases/2026/09/260901010717.htm
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #AgingScience #ImmuneSystem #Inflammation #CellClearance #ReceptorBlocking #YouthfulAging #MiceStudy #OrganHealth #MemoryBoost #AntiAgingResearch
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DATE: August 31, 2026 at 02:00PM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Treadmill running restores memory in Alzheimer’s mice by boosting a key brain pathway
A new study in mice indicates that long-term treadmill exercise might fully reverse memory problems and reduce brain damage associated with Alzheimer’s disease. The research suggests these benefits are tied to the activation of a specific cellular communication pathway that promotes brain health and reduces inflammation. The findings were published in Scientific Reports.
Alzheimer’s disease is a progressive brain disorder characterized by memory loss and a decline in thinking skills. At a cellular level, the disease involves the buildup of toxic protein fragments known as amyloid plaques and tau tangles. These protein clusters disrupt communication between brain cells and trigger chronic inflammation.
Glial cells, which include microglia and astrocytes, act as the brain’s immune system. They initially try to clear away the toxic proteins. But in Alzheimer’s disease, these cells often become stuck in a hyperactive state, which damages healthy neurons and worsens the condition. A 2024 review indicated that physical exercise can help calm this brain inflammation by shifting microglia and astrocytes back into a protective state.
Scientists are still trying to understand exactly how exercise produces these positive changes in the brain. The authors of the new study focused on a specific chemical messenger system known as the brain-derived neurotrophic factor pathway. Brain-derived neurotrophic factor, or BDNF, is a protein that acts like fertilizer for the brain, helping neurons survive, grow, and form new connections.
When this protein binds to its target receptor, called TrkB, it sets off a chain reaction inside the cell that promotes survival and blocks cell death. A 2024 review suggested that physical exercise boosts these protein levels, which helps protect memory during neurodegenerative diseases. Similarly, a 2024 paper proposed that boosting this signaling system can stimulate the repair of myelin, which is the protective coating around nerve fibers that often degrades in Alzheimer’s disease. The researchers wanted to see if the activation of this specific signaling complex could explain the wide-ranging benefits of exercise on Alzheimer’s pathology.
The research, led by Taewan Kim and Hyunsik Kang at Sungkyunkwan University, involved 40 male mice. Half of the mice were genetically modified to develop features of Alzheimer’s disease, including amyloid plaques, tau tangles, and memory deficits. The other half were typical, healthy mice.
Within both the Alzheimer’s model and the healthy groups, the researchers randomly assigned half the mice to an exercise program and half to a sedentary control group. The exercising mice ran on a motorized treadmill for 30 minutes a day, five days a week, for a total of 20 weeks. The speed of the treadmill was gradually increased over the months to maintain a steady physical challenge.
To test cognitive function, the researchers used a water maze at the end of the 20 weeks. The mice had to swim in a small pool to find a hidden platform. The scientists recorded how long it took the mice to learn the platform’s location and how well they remembered it the following day. Afterward, the researchers analyzed the brain tissue and blood of the mice to measure various proteins, inflammatory markers, and cellular changes.
The Alzheimer’s mice that remained sedentary showed severe memory impairments, taking much longer to find the hidden platform than the healthy mice. But the Alzheimer’s mice that exercised performed just as well as the healthy mice, displaying a full recovery of their spatial learning and memory skills.
At the cellular level, the exercising Alzheimer’s mice had substantially lower levels of amyloid plaques and tau tangles in the hippocampus, a brain region vital for memory. The researchers found that treadmill running strongly activated the BDNF-TrkB signaling pathway. This activation was accompanied by a decrease in inflammatory molecules in the blood and brain.
The exercise routine also prompted a shift in the brain’s immune cells. Microglia and astrocytes in the exercising mice transitioned away from a toxic, inflammatory state and toward a restorative, anti-inflammatory state. The findings are in line with research covered by PsyPost in 2021, which found that voluntary physical exercise reversed cognitive impairment and prompted structural changes in astrocytes near amyloid plaques in an Alzheimer’s mouse model.
In addition to calming inflammation, the treadmill running protected the brain’s infrastructure. The exercising Alzheimer’s mice showed improved function in their mitochondria, which are the energy-producing structures inside cells. The researchers also noted a reduction in myelin damage and a decrease in the rate of neuronal cell death compared to the sedentary Alzheimer’s mice. The results align with another study covered by PsyPost in 2025, which observed that regular aerobic exercise reduced tau tangles, amyloid plaques, and myelin damage in naturally aged rats, though the new study specifically examined a genetically modified Alzheimer’s model.
The study provides detailed insights into the brain’s response to physical activity, but there are some caveats to consider. The research was conducted using a mouse model, meaning the findings might not translate directly to human patients with Alzheimer’s disease. The mice also began exercising at four months of age, which corresponds to the early stages of the disease in this specific genetic model. It is unknown if starting an exercise regimen later in the disease’s progression would yield similar benefits.
The researchers focused on changes in protein levels and cellular markers rather than directly blocking the BDNF-TrkB pathway to see if the benefits disappeared. Because of this, it is difficult to determine with absolute certainty that this specific pathway is the sole cause of the improvements. Exercise releases a wide variety of chemical messengers from muscles, which might also travel to the brain and contribute to neuroprotection.
Future research could explore how different types, durations, and intensities of exercise affect brain health in older adults. Scientists also plan to investigate whether these cellular improvements occur in other brain regions beyond the hippocampus.
The study, “Exercise training-induced benefits for Alzheimer’s disease are associated with modulation of the BDNF-TrkB signaling complex,” was authored by Taewan Kim, Jinkyung Cho, and Hyunsik Kang.
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #AlzheimersDisease #BDNFtrkB #BrainHealth #TreadmillExercise #Neuroprotection #InflammationReduction #Microglia #Astrocytes #MemoryRecovery #MiceStudy
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DATE: August 31, 2026 at 07:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Researchers discover preventative immune benefits of a little-known psychedelic compound
URL: https://www.psypost.org/a-psychedelic-compound-primes-the-mouse-brain-to-resist-severe-inflammation/
A small study in mice suggests that administering a psychedelic compound before an immune system challenge can prevent brain inflammation and associated behavioral changes. The findings, published in the journal BMC Neuroscience, hint that these drugs might prime the nervous system to resist future damage.
Neuroinflammation is a biological response where the body’s immune system activates within the brain or spinal cord. While short-term inflammation helps eliminate infections, long-term or excessive immune activity can damage brain tissue. The brain is usually protected from the body’s general immune responses by a specialized cellular boundary. When severe physical stress or infection occurs, signaling molecules can breach this boundary, causing specialized brain cells to initiate a localized immune response.
When the immune system activates, cells release signaling proteins called cytokines. Some cytokines promote inflammation to attack pathogens, while others suppress inflammation to help the body heal. An imbalance leaning toward pro-inflammatory cytokines can disrupt brain circuits and alter an animal’s mood or behavior. This excessive response is a common biological feature in many brain conditions, from Alzheimer’s disease to severe depression.
Psychedelic drugs have gained attention for their ability to treat certain psychiatric conditions, but researchers are also investigating their physical effects on the brain. Many classical psychedelics bind to a specific protein on the surface of brain cells called the serotonin 5-HT2A receptor. Activating this receptor alters perception, but it also appears to influence how immune cells respond to stress. Researchers Michael Fiorillo and Javier González-Maeso of the Virginia Commonwealth University School of Medicine wanted to see if these immune-altering effects could work preventatively.
The researchers began by mapping how the mouse immune system reacts to a specific chemical trigger. They injected a small group of mice with lipopolysaccharide, a molecule found on the outer shell of bacteria. This molecule reliably provokes a strong immune reaction without causing an actual bacterial infection. Following the injection, the team measured chemical markers in the hippocampus, a brain region involved in memory and emotion.
They found that levels of pro-inflammatory cytokines peaked four hours after the injection. Specifically, the proteins interleukin-6 and tumor necrosis factor alpha reached their highest concentrations at this time. This four-hour mark became the target window for evaluating the effects of the psychedelic drug.
In a separate test, the team gave healthy mice varying doses of a psychedelic compound known as DOI. This laboratory chemical activates the same serotonin receptors as drugs like LSD and psilocybin. When they measured brain tissue 24 hours later, they found that DOI alone did not change baseline cytokine levels. The drug did not cause an immune reaction on its own.
Next, the researchers designed an experiment to test DOI as a preventative measure. They injected wild-type mice with either a low or high dose of the psychedelic compound. After waiting 24 hours, they administered the bacterial molecule to trigger systemic inflammation. Four hours after that, they measured cytokine levels in the hippocampus.
Mice that received the low dose of DOI before the immune challenge showed lower levels of interleukin-6 and tumor necrosis factor alpha. Their immune response was notably muted compared to mice that did not receive the psychedelic. The higher dose of the drug did not effectively reduce the inflammatory response, a phenomenon that sometimes occurs when cellular receptors become overwhelmed and shut down.
The team then wanted to know if this protective effect relied entirely on the serotonin 5-HT2A receptor. They repeated the prevention experiment using genetically modified mice that were bred without this specific receptor. In these modified animals, the low dose of DOI failed to prevent the spike in interleukin-6. This outcome indicates that the drug requires the 5-HT2A receptor to suppress this specific inflammatory protein.
However, the drug still successfully reduced levels of tumor necrosis factor alpha in the genetically modified mice. This suggests the psychedelic also interacts with other physiological pathways or different serotonin receptors to manage separate parts of the immune response. The researchers also observed that the modified mice experienced a much stronger overall inflammatory response to the bacterial molecule than unmodified mice. Natural serotonin activity at this receptor normally acts as a biological brake to keep the immune system from overreacting.
To see if the chemical changes in the brain translated to physical actions, the team ran a series of behavioral tests. They placed the mice in an open enclosure monitored by infrared beams to measure general movement and exploration. The bacterial molecule normally causes mice to move less, mimicking the physical lethargy people feel when they are sick.
Pretreating the mice with the low dose of DOI prevented this lethargy. The pretreated animals maintained normal movement levels despite the immune challenge. The team also evaluated the mice using a swimming test that measures passive coping, a behavior often compared to human depression. Mice that received the bacterial molecule spent more time floating passively instead of actively swimming.
Animals given the low dose of DOI beforehand remained active and spent less time floating. The researchers also tracked the animals’ body weight over a single week. The immune challenge typically causes severe weight loss, but the psychedelic treatment lessened this physical toll. The pretreated mice recovered their normal weight faster than the untreated control group.
Finally, the researchers looked for links between the chemical markers in the brain and the animals’ physical behavior. They found that higher levels of the inflammatory cytokine interleukin-6 matched up with increased passive behavior in the swimming test. Conversely, higher levels of two other cytokines associated with cellular healing aligned with more active swimming. This chemical shift points toward a more resilient biological state.
While these results offer a look at how psychedelics might shield the brain, the research relied on a single strong immune trigger. This acute response does not fully capture the persistent, low-grade inflammation seen in human neurodegenerative and psychiatric diseases. Additionally, the study evaluated whole sections of the hippocampus rather than looking at individual cell types. It remains unknown exactly which immune or nervous system cells are actually suppressing the inflammation.
The bacterial molecule and the drug were injected into the animals’ bodies rather than directly into the brain. It is possible that the psychedelic suppressed the immune response in the bloodstream first, which then reduced the secondary inflammation in the brain. The genetically modified mice used in the study lacked the serotonin receptor for their entire lives, which might have caused developmental changes that independently altered their baseline immune system.
All the experiments were conducted using male mice. Future research will need to include female animals to determine if these preventative immune effects apply equally across sexes. Scientists also need to test other psychedelic compounds to see if they offer similar protective benefits.
The study, “Pretreatment with the psychedelic DOI mitigates LPS-induced hippocampal inflammation and behavioral impairments in mice,” was authored by Michael Fiorillo and Javier González-Maeso.
URL: https://www.psypost.org/a-psychedelic-compound-primes-the-mouse-brain-to-resist-severe-inflammation/
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #PsychedelicsAndImmuneHealth #DOIPrevention #5HT2AReceptor #Neuroinflammation #HippocampusProtection #LPSInflammation #Cytokines #NeuropsychiatricResearch #MiceStudy #BrainImmuneInteraction
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DATE: August 27, 2026 at 12:00PM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: The hallucinogenic plant Salvia divinorum relieves facial pain, study finds
URL: https://www.psypost.org/a-hallucinogenic-mint-plant-relieves-facial-pain-in-mice/
A compound extracted from a hallucinogenic mint plant reduces facial pain in mice by interacting with specific receptors in the nervous system. The research provides a biological basis for the plant’s historical use in indigenous medicine and suggests new avenues for treating persistent nerve pain. The study was published in the Journal of Ethnopharmacology.
Trigeminal pain, also known as orofacial pain, originates in the sensory nerves of the face and can be highly disruptive to daily life. For a large portion of the population, this type of discomfort persists despite standard medical treatments and pain relievers. In the Cañada region of Oaxaca, Mexico, traditional healers address this condition by preparing an infusion from the leaves of the *Salvia divinorum* plant.
The plant is a member of the mint family and is widely known for its fast-acting hallucinogenic effects. During spiritual ceremonies, healers use large quantities of the fresh leaves to induce visions. However, when treating physical ailments like headaches or rheumatism, they prepare a much weaker tea from only a few leaves. This ethnobotanical history inspired scientists to take a closer look at how the plant acts on the body’s pain pathways.
To understand how this plant alters pain perception without inducing heavy hallucinations, researchers Geovanna Nallely Quiñonez-Bastidas, Andrés Navarrete, and their colleagues investigated its primary active compound. The chemical, called salvinorin A, is known to produce mind-altering effects by binding to specific opioid receptors in the brain. The research team suspected the chemical might also interact with two other prominent sensory structures in the nervous system.
One target is the cannabinoid type 1 receptor, which is part of the system that responds to the active ingredients in cannabis. The other is the transient receptor potential vanilloid 1, a cellular channel involved in sensing heat and pain. Both of these receptors are heavily concentrated in the sensory nerves of the face. This makes them logical targets for investigating how a traditional plant medicine might soothe orofacial pain.
To test the plant’s pain-relieving properties, the researchers conducted a small study using laboratory mice. They prepared a concentrated extract from dried *Salvia divinorum* leaves and also isolated the purified salvinorin A compound. They then injected a mild chemical irritant called formalin into the upper lip of the mice to simulate trigeminal pain. This minor irritation prompts the animals to repeatedly rub their faces, providing a measurable behavioral sign of discomfort.
The researchers observed the animals after administering varying doses of either the whole plant extract or the purified chemical. Both the plant extract and the purified salvinorin A reduced the amount of time the mice spent rubbing their faces. The purified chemical was highly potent, requiring only about one-tenth the dose of the full extract to achieve the exact same level of pain relief. This indicates that salvinorin A is the primary component driving the plant’s biological effects on pain.
The team wanted to isolate the specific biological pathways involved in this response. They injected a new group of mice with chemical blockers that temporarily disable specific nervous system receptors. Some mice received a blocker designed specifically for the cannabinoid receptor. Other mice received a blocker targeted at the vanilloid receptor. After disabling these specific cellular targets, the scientists administered the plant compound and exposed the mice to the lip irritant.
When either the cannabinoid or vanilloid receptors were chemically blocked, salvinorin A lost its ability to relieve the facial pain. The researchers also tested blockers for two other common nervous system pathways, but disabling those did not stop the compound from working. These outcomes demonstrate that the compound relies directly on the cannabinoid and vanilloid receptors to suppress pain signals in the face.
The researchers then performed a laboratory test using isolated tissue to biologically confirm these receptor interactions. They extracted the esophagus and its connected vagus nerve from rats. By applying mild electrical pulses, they prompted the nerve to trigger rhythmic muscle contractions in the esophagus tissue. The team then applied salvinorin A to the tissue bath to observe its effect on nerve transmission.
Applying the compound effectively stopped the nerve from triggering the muscle contractions. When the scientists added the same chemical blockers used in the live mouse experiment, the nerve impulses and muscle contractions returned to normal. This isolated tissue test provided direct physical evidence that salvinorin A alters nerve activity through the specified sensory receptors.
Finally, the researchers evaluated whether the pain-relieving doses of salvinorin A produced other behavioral side effects. They subjected the mice to a battery of tests designed to measure anxiety, motor coordination, sedation, and depression-like behavior. To measure anxiety, they observed how much time the mice spent exploring open areas versus hiding in enclosed spaces. For motor skills, they tracked the animals’ ability to walk on a rotating cylinder.
The compound did not alter the animals’ anxiety levels. Changes in the amount of time the mice spent in open areas were not statistically significant compared to untreated mice. The animals treated with the compound also performed just as well on the rotating cylinder, showing no signs of physical impairment. However, the animals did exhibit certain noticeable behavioral changes in other environments.
In a test that involves placing the mice in a cylinder of water, the treated animals spent more time floating motionlessly rather than actively swimming. In a separate observation test, the treated mice were less likely to rear up on their hind legs to explore a new enclosure. The researchers interpreted these reduced activity levels as signs of mild depressive and sedative side effects.
While the compound demonstrates a powerful ability to block facial pain, its sedative and depressive side effects present hurdles for daily medical use. The mind-altering properties of the plant, which are heavily documented at higher doses, also complicate its potential development into a standard therapeutic drug.
Future research will likely focus on evaluating the chemical in different models of nerve damage. Scientists will also need to test modifications of the compound to see if they can isolate the pain-relieving benefits while reducing the unwanted psychological effects.
The study, “Antinociceptive effect of salvinorin A from the extract of Salvia divinorum in formalin-evoked trigeminal pain behavior in mice: Underlying mechanisms,” was authored by Geovanna Nallely Quiñonez-Bastidas, Eva Daysi Tixta-Ramírez, José Luis Balderas-López, Paola Andrea Vargas-Durán, Araceli Pérez-Vásquez, and Andrés Navarrete.
URL: https://www.psypost.org/a-hallucinogenic-mint-plant-relieves-facial-pain-in-mice/
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #SalviaDivinorum #SalvinorinA #FacialPainRelief #TrigeminalPain #PainResearch #CannabinoidReceptor #VanilloidReceptor #Ethnopharmacology #NervePainTreatment #MiceStudy
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DATE: August 27, 2026 at 12:46AM
SOURCE: SCIENCE DAILY MIND-BRAIN FEEDTITLE: Scientists discover a brain “brake” that can shut down chronic pain
URL: https://www.sciencedaily.com/releases/2026/08/260826055442.htm
Researchers discovered a brain-based “brake” that can shut down chronic nerve pain in mice by calming an overactive pain circuit. Targeting this system more precisely could one day lead to powerful pain relief without affecting opioid receptors throughout the entire body.
URL: https://www.sciencedaily.com/releases/2026/08/260826055442.htm
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DATE: August 26, 2026 at 03:28AM
SOURCE: SCIENCE DAILY PSYCHIATIRY FEEDTITLE: Childhood trauma may leave a lasting “scar” inside brain cells
URL: https://www.sciencedaily.com/releases/2026/08/260823094151.htm
Early-life stress may physically alter how DNA is packaged in the brain, leaving stress-related genes primed to activate more easily years later. In mice, researchers were able to block this effect, preventing the heightened anxiety and stress sensitivity that otherwise appeared in adulthood.
URL: https://www.sciencedaily.com/releases/2026/08/260823094151.htm
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DATE: August 26, 2026 at 03:28AM
SOURCE: SCIENCE DAILY MIND-BRAIN FEEDTITLE: Childhood trauma may leave a lasting “scar” inside brain cells
URL: https://www.sciencedaily.com/releases/2026/08/260823094151.htm
Early-life stress may physically alter how DNA is packaged in the brain, leaving stress-related genes primed to activate more easily years later. In mice, researchers were able to block this effect, preventing the heightened anxiety and stress sensitivity that otherwise appeared in adulthood.
URL: https://www.sciencedaily.com/releases/2026/08/260823094151.htm
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DATE: August 23, 2026 at 11:15AM
SOURCE: SCIENCE DAILY MIND-BRAIN FEEDTITLE: A major Alzheimer’s risk gene may shrink brain cells years before symptoms
URL: https://www.sciencedaily.com/releases/2026/08/260821012234.htm
Researchers have uncovered a possible reason why the Alzheimer’s risk gene APOE4 can disrupt the brain long before memory problems begin. In mice, APOE4 increased a protein called Nell2, shrinking neurons and making memory circuits unusually active. That early hyperactivity predicted worse memory later in life. Reducing Nell2 in adult mice reversed the abnormal changes, raising hopes for a new way to intervene before Alzheimer’s progresses.
URL: https://www.sciencedaily.com/releases/2026/08/260821012234.htm
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DATE: August 22, 2026 at 10:46PM
SOURCE: SCIENCE DAILY MIND-BRAIN FEEDTITLE: Quitting alcohol may prime the brain for relapse
URL: https://www.sciencedaily.com/releases/2026/08/260822015148.htm
Mice that developed compulsive drinking after alcohol abstinence showed more than double the activity in a brain region associated with stress and addiction. Because the signal appeared before they drank again, researchers think it could eventually help predict who is most at risk of relapse.
URL: https://www.sciencedaily.com/releases/2026/08/260822015148.htm
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DATE: August 20, 2026 at 06:59PM
SOURCE: SCIENCE DAILY MIND-BRAIN FEEDTITLE: Ozempic does something unexpected to the brain’s hunger neurons
URL: https://www.sciencedaily.com/releases/2026/08/260820002436.htm
Ozempic may work in the brain in almost the opposite way scientists expected, activating hunger-linked neurons that appear essential for sustaining fat loss. The surprising discovery in mice could reveal new targets for developing even more effective obesity drugs.
URL: https://www.sciencedaily.com/releases/2026/08/260820002436.htm
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DATE: August 16, 2026 at 09:01PM
SOURCE: SCIENCE DAILY PSYCHOLOGY FEEDTITLE: A little-known protein may be fueling Alzheimer’s — and scientists found a way to block it
URL: https://www.sciencedaily.com/releases/2026/08/260814235856.htm
An experimental Alzheimer’s compound prevented damaging protein clumps from forming in the brains of mice, helping nerve cells survive longer and reducing amyloid buildup. The treatment also appeared to improve heart health and slow some signs of aging, raising hopes for an entirely new way to combat dementia.
URL: https://www.sciencedaily.com/releases/2026/08/260814235856.htm
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DATE: August 16, 2026 at 09:01PM
SOURCE: SCIENCE DAILY MIND-BRAIN FEEDTITLE: A little-known protein may be fueling Alzheimer’s — and scientists found a way to block it
URL: https://www.sciencedaily.com/releases/2026/08/260814235856.htm
An experimental Alzheimer’s compound prevented damaging protein clumps from forming in the brains of mice, helping nerve cells survive longer and reducing amyloid buildup. The treatment also appeared to improve heart health and slow some signs of aging, raising hopes for an entirely new way to combat dementia.
URL: https://www.sciencedaily.com/releases/2026/08/260814235856.htm
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DATE: August 12, 2026 at 08:43AM
SOURCE: SCIENCE DAILY MIND-BRAIN FEEDTITLE: The adult brain can repair itself better than scientists thought
URL: https://www.sciencedaily.com/releases/2026/08/260812015158.htm
The adult brain may be far better at repairing itself than scientists once believed. In mice, researchers discovered a special group of support cells called astrocytes that respond to damaged brain tissue by rebuilding lost cellular networks. Rather than simply moving into the injured area, these cells perform a remarkable maneuver: they create new nuclei and send them traveling through long cellular extensions to repopulate damaged regions.
URL: https://www.sciencedaily.com/releases/2026/08/260812015158.htm
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Single Dose of Frog-Derived Gut Bacterium Eradicates 100% of Tumors in Mice
https://www.thefocalpoints.com/p/new-study-frog-derived-gut-bacterium
#HackerNews #FrogBacterium #TumorEradication #CancerResearch #MiceStudy #GutHealth