#psilocybin — Public Fediverse posts
Live and recent posts from across the Fediverse tagged #psilocybin, aggregated by home.social.
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@PsychedelicInstitute How many more of these studies do we need before they loosen the reins?
#Psilocybin knocked down all the mental and emotional walls I had built up and allowed me to release a giant ball of pain I'd been clinging to for a quarter century. And it did it in the span of 24 hours. I am literally a new me.
Nowadays I micro-dose four days a week. It just makes my day better. I laugh more, I smile more, and the stress of the day becomes manageable.
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New research shows how psychedelics reorganise the patterns in your brain
#Science #Psychology #Nature
#Psilocybin #Psychedelics #Brain #MentalHealth #BrainImaging #MRI #EEG #Consciousness #AIResearch #BrainResearch #Neuroscience #HealthResearch #MedicalScience
https://the-14.com/new-research-shows-how-psychedelics-reorganise-the-patterns-in-your-brain/ -
A real-world study of Oregon's nonmedical psilocybin program shows promise, Will Stone reports. Find this article and more at canadahealthwatch.ca #CdnHealth #Psilocybin
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DATE: August 16, 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: Psychedelic drug calms hyperactive brain cells linked to chronic pain
URL: https://www.psypost.org/a-single-dose-of-psilocybin-relieves-chronic-pain-and-depression-in-mice/
A single dose of the psychedelic compound psilocybin can rapidly relieve both chronic pain and the symptoms of anxiety and depression that often accompany it. The drug achieves this dual effect by calming hyperactive brain circuits associated with these linked conditions. The research was published in Nature Neuroscience.
Chronic pain rarely exists in isolation. People who suffer from persistent physical pain often develop mood disorders like anxiety and depression. These conditions can feed into one another, making the pain feel worse and making the depression harder to treat. Standard medical treatments usually address the physical pain and the mood symptoms separately, often with limited success.
Researchers suspect these conditions share an underlying physical root in the brain. Brain scans of individuals with chronic pain and depression often show abnormal activity in the anterior cingulate cortex. This region of the brain helps process emotions and the unpleasantness of pain.
Psilocybin is the primary psychoactive ingredient found in magic mushrooms. Once ingested, the body converts it into an active molecule called psilocin. Psilocin binds to serotonin receptors in the brain, which are the same receptors targeted by many standard antidepressant medications.
Recent clinical trials have shown that psilocybin can provide lasting relief for severe depression. Separate observations suggest it might also help with chronic nerve pain. University of Pennsylvania researchers Joseph Cichon, Ahmad Hammo, and Stephen Wisser wanted to see if a single treatment could target the shared brain circuits of both conditions at the same time.
To study this, the research team first established chronic pain in laboratory mice using two different methods. One group of mice received a minor surgical nerve injury to simulate long-lasting nerve pain. Another group received a specialized injection in their paw to create persistent inflammatory pain.
After a few weeks, both groups of mice displayed severe sensitivity to a light physical touch. They also began to show behaviors that researchers use to gauge anxiety and depression in rodents. For example, they spent less time exploring open, exposed areas, and they showed less motivation to keep moving when placed in water.
The researchers then gave the mice a single systemic injection of psilocybin. The next day, the mice showed a complete reversal of their physical pain sensitivity. Their mood-related behaviors also returned to normal baseline levels. This restorative effect lasted for at least twelve days, which was the end of the testing period.
To verify that the psilocybin was actually relieving the negative experience of pain, the team used a behavioral test involving two connected rooms. The mice were given psilocybin in one specific room and a plain saline solution in the other.
When given the freedom to choose, the mice with chronic pain strongly preferred to spend time in the room where they had received psilocybin. Healthy mice without pain did not show this preference. This indicates that the mice associated the environment with the relief of their discomfort.
Pain signals travel from the body, up the spinal cord, and into the brain. The researchers needed to find out exactly where the drug was acting to provide relief. They injected psilocin directly into the lower spinal cords of a group of mice with nerve pain. This local spinal treatment did not improve the animals’ pain or mood behaviors.
Next, they injected the psilocin directly into the anterior cingulate cortex of the brain. This direct brain application rapidly reversed both the physical pain sensitivity and the signs of depressed mood. This result suggests that the drug works by altering networks in the higher brain centers rather than blocking pain signals at the spinal level.
To observe this brain activity in real time, the team used a technique called two-photon calcium imaging. This allowed them to look at individual brain cells in the anterior cingulate cortex of awake mice.
They found that mice with chronic pain had abnormally high levels of spontaneous cellular activity in this brain region. When the researchers applied psilocin to the area, it rapidly suppressed this erratic hyperactivity. The overactive cells quieted down to match the activity levels seen in healthy mice.
Psilocin interacts with several types of serotonin receptors, specifically ones known as 5-HT2A and 5-HT1A. To figure out which receptors were responsible for the healing effect, the team gave the mice drugs that block these specific receptors before administering the psilocybin.
Blocking either the 5-HT2A receptor or the 5-HT1A receptor completely stopped the psilocybin from working. The mice remained in pain and continued to show depressed behaviors. This demonstrates that psilocybin requires access to both of these serotonin receptor types simultaneously to initiate its healing effects.
In pharmacology, a full agonist is a drug that turns a receptor on completely. A partial agonist, like psilocin, only turns it on partially. The researchers tested what would happen if they used different drugs to fully activate the 5-HT2A and 5-HT1A receptors in the mice.
Activating these receptors fully, even at the same time, failed to replicate the broad therapeutic effects of psilocybin. The mice did not experience the same comprehensive relief from pain and mood issues. The researchers suspect that the partial activation provided by psilocin creates a specific, balanced modulation of brain cells that full activation cannot achieve.
While these animal studies offer a detailed look at brain circuitry, mice are not humans. Brain structures and the subjective experience of pain differ between species. It is not yet known if the specific dosage that provided relief in mice will translate safely and effectively to human patients.
The researchers tracked the mice for twelve days after the single dose. It remains unseen exactly how long the pain relief might last beyond that window.
Future studies will need to explore how this brief chemical intervention translates into long-term physical changes in the brain. The authors suggest that calming the hyperactive brain cells might allow the brain to physically rewire itself, breaking the cycle of chronic pain and depression over time.
The study, “Single-dose psilocybin rapidly and sustainably relieves allodynia and anxiodepressive-like behaviors in mouse models of chronic pain,” was authored by Ahmad Hammo, Stephen Wisser, and Joseph Cichon.
URL: https://www.psypost.org/a-single-dose-of-psilocybin-relieves-chronic-pain-and-depression-in-mice/
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #psilocybin #chronicpain #anxiodepressive #serotoninreceptors #5HT2A #5HT1A #neuroscience #NatureNeuroscience #painrelief #psychedelictherapy
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Psilocybin’s Lasting Impact
A growing body of research is reshaping how scientists understand psychedelics, not as fleeting, mind-altering experiences, but as catalysts for longer-term biological change
https://neurodoctor.com/2026/08/03/psilocybins-lasting-impact/
#psychedelics #Psilocybin #ketamine #Depression #PTSD -
DATE: July 30, 2026 at 06:00AM
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: Neuroscientists just upended a core assumption about how psychedelics alter brain function
Recent research published in the Proceedings of the National Academy of Sciences suggests that psychedelic substances change how brain activity travels across the surface of the brain. The study provides evidence that drugs like LSD, psilocybin, and MDMA reliably reduce the flow of information traveling up into a core brain network associated with self-reflection. These findings offer a new biological explanation for both the therapeutic potential and the psychological risks of using psychedelics to treat mental health conditions.
The default mode network is a collection of interconnected brain regions that are highly active when a person is resting and thinking about themselves. Scientists link this network to introspection, daydreaming, and maintaining a rigid sense of self. In many mental health disorders, such as depression or schizophrenia, the default mode network tends to function abnormally. Because of this connection, researchers want to know exactly how potential psychiatric treatments impact this specific network.
“Psychedelic use is growing faster than our understanding of how these drugs impact the brain, particularly at the level of large-scale brain networks,” said Adam Pines, a postdoctoral scholar at Stanford University, who led the study alongside the study’s senior author, Leanne M. Williams. “Clinically, these unresolved questions limit our ability to know which patients are likely to benefit from psychedelic treatments, and which are at risk of harm.”
Previous studies usually measured brain activity as if it were fixed in place. They looked at average activity in stationary regions over time instead of tracking how signals physically move across the brain tissue.
Brain activity constantly travels in specific directions, either from lower-level sensory areas up to higher-level thinking areas, or vice versa. The upward movement is called bottom-up processing, which involves reacting to basic sensory input. The downward movement is known as top-down processing, where the brain applies past experiences and expectations to interpret incoming information.
“Existing theories on how psychedelics work tend to disagree on a core point: whether psychedelics increase or decrease ‘bottom-up’ brain activity (activity moving from lower-order to higher-order brain areas),” Pines said. “From our perspective, this core premise had not been systematically tested.”
To test this premise, the researchers adapted an analytical method called optical flow. This technique is typically used in computer vision to track the movement of physical objects across video frames. By applying this technique to brain scans, the researchers could evaluate the directional flow of brain activity frame by frame, capturing the exact movement of signals across the cortical surface.
The researchers combined data from four independent studies to test how different psychedelics impact brain activity flow. “Drawing conclusive evidence from psychedelic studies is notoriously difficult,” Pines said. “We tried to establish our results beyond reasonable doubt by replicating our findings across nine different case-control comparisons, involving four datasets and two completely different neuroimaging technologies.”
The first three studies involved human participants who received a specific drug and underwent functional magnetic resonance imaging. This type of brain scan, often called fMRI, measures changes in blood flow to detect active brain areas. Before running their optical flow analysis, the authors masked out segments of data interrupted by head motion to ensure their measurements were highly accurate.
In the first study, fourteen healthy adult participants received either a placebo, eighty milligrams of MDMA, or one hundred and twenty milligrams of MDMA. MDMA is a synthetic substance that alters mood and perception. Participants completed multiple scanning sessions across different days, allowing researchers to compare their brain activity with and without the active drug.
The second study evaluated the effects of psilocybin, the active hallucinogenic compound found in magic mushrooms. Six healthy participants underwent numerous fMRI scans. During some sessions, they received twenty-five milligrams of psilocybin. On other days, they received either no drug or an active placebo called methylphenidate, a stimulant medication that mimics the physical arousal caused by psilocybin.
The third study focused on LSD, a powerful chemical that alters perception and thought. Eighteen healthy participants received an intravenous infusion of either LSD or a saline placebo. Following a short acclimatization period, they completed about one hour of fMRI scanning to capture their brain activity under the influence of the substance.
The fourth study involved an entirely different species and measurement technique. Fourteen mice were administered LSD, a sedative called diazepam, or another sedative called dexmedetomidine. Instead of using fMRI, the scientists measured the mouse brain activity using widefield calcium imaging. This technique uses fluorescent markers to directly observe the electrical activity of neurons across the brain surface, providing a different perspective on brain function.
Across all four datasets, the authors looked at two main features of brain signals moving within the default mode network. First, they calculated the magnitude, which is the total volume and strength of the traveling brain waves. Second, they measured directionality, specifically looking at the proportion of signals traveling in a bottom-up direction from sensory regions into the default mode network.
The researchers found that all the tested psychedelics significantly reduced the overall magnitude of cortical activity propagations in the default mode network. In the first study, MDMA lowered the strength of these traveling signals compared to both placebo and baseline scans. The exact same pattern appeared in the second study for psilocybin and the third study for LSD.
When observing the mice in the fourth study, the authors noticed a similar reduction in signal magnitude after administering LSD. The active sedatives given to the mice produced the opposite effect, increasing the magnitude of brain signal movement. This suggests that the reduction in traveling waves is a specific feature of psychedelics rather than a general effect of taking any psychoactive drug.
In addition to shrinking the magnitude of these signals, psychedelics altered the direction of their travel. The human studies showed that MDMA, psilocybin, and LSD all reduced the percentage of signals moving in a bottom-up direction. Instead of information flowing freely from sensory areas up into the default mode network, the overall balance of activity shifted away from bottom-up processing.
The mouse study replicated this directional shift, as LSD significantly decreased bottom-up propagations in the mouse brains. Interestingly, the psilocybin study showed that this attenuation of bottom-up directionality persisted for days after the initial dosage. Scans taken within two days of the psilocybin sessions still exhibited proportionately fewer bottom-up propagations.
The scientists also checked whether these movement changes were linked to the subjective psychological effects of the drugs. In the human studies, participants filled out comprehensive questionnaires about their experiences. The scientists found that greater reductions in bottom-up signaling correlated with more intense negative feelings, such as the dread of losing one’s sense of self and feelings of impaired control.
The results went against the original expectations of the research team. “How psychedelics impact large-scale brain function is not settled science,” Pines told PsyPost. “Our study challenges one of the field’s core assumptions. Many researchers, myself included, expected psychedelics to increase ‘bottom-up’ activity.”
Pines noted that the actual data told a different story. “Instead, we found the opposite,” Pines said. “However, like any study, there are caveats and limitations that come along with this new evidence.”
One prospective issue is the way the researchers interpreted the data at a broad level. “In our human data, we described a group-level effect rather than something that occurs 100% of the time for every individual every time they ingest psychedelics,” Pines said. “This is a standard practice for human neuroimaging studies, but it’s worth keeping in mind that the impact of psychedelics on individual people can be quite variable.”
The concept of bottom-up processing also comes with its own complexities. “Scientists still don’t fully understand what we call bottom-up activity, or the different ways it can occur,” Pines said. “Analytically, we only measured bottom-up activity in one way rather than comprehensively resolving all possible bottom-up activity in the brain.”
The researchers acknowledge that they had to narrow their focus to run the optical flow analyses. “While we had to be reductionistic to evaluate our questions of interest, there are undoubtedly more nuanced aspects of bottom-up and top-down activity that are yet to be discovered in psychedelic research and neuroscience broadly,” Pines said.
These brain wave changes might explain why psychedelics have specific therapeutic effects. For instance, ruminative depression involves excessive, automatic negative thoughts, which researchers link to an overabundance of bottom-up cortical propagations. By reducing these bottom-up signals, psychedelics might interrupt the automatic negative thought loops associated with depression.
A reduction in bottom-up processing could also pose risks for certain vulnerable populations. People at risk for psychosis already experience impaired bottom-up processing, often relying too heavily on top-down expectations, which can lead to hallucinations. Taking a psychedelic might exacerbate this existing imbalance, providing a biological explanation for why these drugs can trigger psychotic episodes in susceptible individuals.
The researchers plan to expand this analytical approach beyond psychedelics to other chemical compounds. “Our lack of understanding of large-scale brain function is not unique to psychedelic drugs,” Pines said. “Although decades of thorough research have revealed a lot about how alcohol, nicotine, and neurologically-active pharmaceuticals operate on individual neurons, our knowledge of how they impact large-scale brain function is quite limited.”
Applying this knowledge could eventually help doctors provide more personalized medical care. “If we can clarify the impacts of neurologically-active substances broadly, we can better anticipate the effects of any given therapeutic drug on individual psychiatric patients and tailor prescriptions accordingly,” Pines said. “This gives us more confidence in our findings, but doesn’t mean that the question is closed. Further study is still needed.”
The study, “Psychedelics disrupt hierarchical cortical propagations in the default mode network of humans and mice,” was authored by Adam R. Pines, Xue Zhang, John Kochalka, Sam S. Vesuna, Isaac V. Kauvar, Divya Rajasekharan, T. Rick Reneau, Teddy J. Akiki, Laura M. Hack, Joshua S. Siegel, and Leanne M. Williams.
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #PsychedelicsBrainScience #DefaultModeNetwork #BottomUpProcessing #PsychedelicsAndMentalHealth #MDMA #Psilocybin #LSD #NeuroscienceResearch #BrainConnectivity #OpticalFlowNeuroimaging