#psychedelictherapy — Public Fediverse posts
Live and recent posts from across the Fediverse tagged #psychedelictherapy, aggregated by home.social.
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DATE: August 20, 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: New study tracks oxytocin spikes in MDMA therapy trials
URL: https://www.psypost.org/meta-analysis-confirms-mdma-triggers-sustained-oxytocin-release/
The psychoactive drug MDMA temporarily increases levels of the social hormone oxytocin in human subjects, with levels peaking a few hours after use. These findings might help researchers time therapeutic interventions during clinical trials for psychiatric conditions like post-traumatic stress disorder. The research was published in Neuroscience and Biobehavioral Reviews.
The drug 3,4-methylenedioxymethamphetamine, commonly known as MDMA, is classified as an entactogen. This designates it as a psychoactive substance that heavily alters emotional processing. People who take the substance often report enhanced feelings of closeness, empathy, and social unity.
In recent years, MDMA has become the subject of clinical trials for treating post-traumatic stress disorder, commonly called PTSD. Therapists suggest that the drug helps patients build an emotional bond with their doctors. It reduces anxiety related to social interactions and helps people process perceived emotional threats.
Researchers suspect a primary biological mechanism behind these prosocial effects is the release of oxytocin. Oxytocin is a chemical messenger produced in the hypothalamus, a region deep within the brain. It acts as both a local brain signaling molecule and a hormone that circulates throughout the body.
The hormone is best known for its role in childbirth and lactation, but it also regulates social behaviors. Elevated levels of oxytocin are linked to increased empathy, generosity, and trust, particularly among people within the same social group.
MDMA initiates its effects by causing the brain to release a flood of monoamines. These are chemical messengers that include serotonin, dopamine, and norepinephrine.
The sudden surge of serotonin activates specific receptors on neurons in the hypothalamus. Animal models demonstrate that this receptor activation directly triggers the release of oxytocin into the bloodstream and central nervous system.
Medical professionals have tried administering oxytocin directly via nasal sprays to treat social anxiety and similar conditions. However, the nasal spray has a very short active period in the bloodstream, disappearing in just a few minutes.
MDMA, by contrast, has a much longer active window. It promotes a robust release of the body’s own naturally produced oxytocin. This creates a sustained social effect that is better suited for long psychotherapy sessions.
While individual studies have shown that MDMA triggers the release of oxytocin, results have varied widely. Lead author Anna Vaslavski, a researcher at Bar-Ilan University, and her colleagues noticed a gap in the literature. No previous research had systematically gathered and analyzed these disparate studies to figure out exactly how the drug influences oxytocin levels across different times, doses, and demographic groups.
To find answers, the research team conducted a meta-analysis. This is a statistical technique that pools data from multiple independent studies to identify overall trends. The team searched academic databases to find peer-reviewed studies that administered MDMA to human subjects and measured their oxytocin levels.
They identified ten qualifying studies containing a total of 39 effect size estimates. The original studies used varying doses of MDMA, ranging from 75 to 150 milligrams. The researchers also measured oxytocin from blood or urine samples at different time intervals.
The team analyzed this pooled data, looking specifically at three modifying variables. They tested whether the amount of the drug, the time of measurement, or the sex of the participants altered the amount of oxytocin released.
Time emerged as a modifying factor, showing a curvilinear relationship with hormone levels. After a person took MDMA, their oxytocin levels rose steadily. The levels reached their highest point between 150 and 200 minutes after administration.
Following this peak, oxytocin concentrations began to decline. Some studies noted that levels remained slightly elevated above their baseline even five hours after the drug was taken.
The analysis did not find a statistically significant relationship between the dose of MDMA and the resulting oxytocin levels. The varied dosing strategies used in the original ten studies might explain this lack of an effect. Some studies gave all participants a flat dose, while others adjusted the amount based on a person’s body weight.
The team also found a slight trend regarding the sex of the participants. The results suggested that studies with a higher proportion of female subjects tended to record smaller increases in oxytocin. However, this finding was not statistically significant and requires more targeted testing to confirm.
Readers should exercise caution when interpreting blood or urine oxytocin levels as a direct reflection of brain activity. Oxytocin in the bloodstream does not easily cross the blood-brain barrier, meaning peripheral levels might not perfectly mirror the amounts acting directly on brain circuits.
Still, recent physiological studies suggest that circulating oxytocin can influence the brain indirectly. The hormone can stimulate the vagus nerve, a major neural pathway connecting the body’s internal organs to the brainstem. This vagal pathway might carry the social and emotional signals generated by peripheral oxytocin into the central nervous system.
The meta-analysis also revealed a high degree of unexplained variance among the ten studies. The statistical models showed that differences in time, dose, and sex only accounted for about a quarter of the variation in the results. This indicates that other unmeasured biological factors are influencing how much oxytocin the body releases in response to MDMA.
The potential difference in how males and females respond to the drug might be tied to estrogen. Estrogen is known to regulate how sensitive cells are to oxytocin.
Because the analysis relied on existing published data, the research team could not isolate female-only groups or control for the use of hormonal birth control. These missing details leave the exact nature of the sex difference an open question. Differences in body mass index or the menstrual cycle could potentially alter how a person reacts to the drug.
Methodological differences in how the original researchers processed their biological samples might also have skewed the overall numbers. Oxytocin levels can appear vastly different depending on whether researchers use advanced extraction techniques to isolate the hormone from blood plasma.
Moving forward, scientists need to standardize how they administer MDMA and measure oxytocin. Implementing consistent dosing based on body weight and utilizing uniform extraction methods will yield more reliable data.
The researchers also noted evidence of publication bias in the available literature. Small studies with larger margins of error tended to report disproportionately high oxytocin effects. Conducting studies with a large sample size will help correct this imbalance and verify the true strength of the drug’s impact on the hormonal system.
The study, “The effect of MDMA administration on oxytocin concentration levels: systematic review and a multilevel meta-analysis in humans,” was authored by Anna Vaslavski, Anna Harwood-Gross, Salomon Israel, and Leehe Peled-Avron.
URL: https://www.psypost.org/meta-analysis-confirms-mdma-triggers-sustained-oxytocin-release/
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #MDMA #Oxytocin #PTSDtherapy #Neuroscience #MentalHealthResearch #SocialChemistry #PsychedelicTherapy #OxytocinPeak #ClinicalTrials #MetaAnalysis
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DATE: August 20, 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: New study tracks oxytocin spikes in MDMA therapy trials
URL: https://www.psypost.org/meta-analysis-confirms-mdma-triggers-sustained-oxytocin-release/
The psychoactive drug MDMA temporarily increases levels of the social hormone oxytocin in human subjects, with levels peaking a few hours after use. These findings might help researchers time therapeutic interventions during clinical trials for psychiatric conditions like post-traumatic stress disorder. The research was published in Neuroscience and Biobehavioral Reviews.
The drug 3,4-methylenedioxymethamphetamine, commonly known as MDMA, is classified as an entactogen. This designates it as a psychoactive substance that heavily alters emotional processing. People who take the substance often report enhanced feelings of closeness, empathy, and social unity.
In recent years, MDMA has become the subject of clinical trials for treating post-traumatic stress disorder, commonly called PTSD. Therapists suggest that the drug helps patients build an emotional bond with their doctors. It reduces anxiety related to social interactions and helps people process perceived emotional threats.
Researchers suspect a primary biological mechanism behind these prosocial effects is the release of oxytocin. Oxytocin is a chemical messenger produced in the hypothalamus, a region deep within the brain. It acts as both a local brain signaling molecule and a hormone that circulates throughout the body.
The hormone is best known for its role in childbirth and lactation, but it also regulates social behaviors. Elevated levels of oxytocin are linked to increased empathy, generosity, and trust, particularly among people within the same social group.
MDMA initiates its effects by causing the brain to release a flood of monoamines. These are chemical messengers that include serotonin, dopamine, and norepinephrine.
The sudden surge of serotonin activates specific receptors on neurons in the hypothalamus. Animal models demonstrate that this receptor activation directly triggers the release of oxytocin into the bloodstream and central nervous system.
Medical professionals have tried administering oxytocin directly via nasal sprays to treat social anxiety and similar conditions. However, the nasal spray has a very short active period in the bloodstream, disappearing in just a few minutes.
MDMA, by contrast, has a much longer active window. It promotes a robust release of the body’s own naturally produced oxytocin. This creates a sustained social effect that is better suited for long psychotherapy sessions.
While individual studies have shown that MDMA triggers the release of oxytocin, results have varied widely. Lead author Anna Vaslavski, a researcher at Bar-Ilan University, and her colleagues noticed a gap in the literature. No previous research had systematically gathered and analyzed these disparate studies to figure out exactly how the drug influences oxytocin levels across different times, doses, and demographic groups.
To find answers, the research team conducted a meta-analysis. This is a statistical technique that pools data from multiple independent studies to identify overall trends. The team searched academic databases to find peer-reviewed studies that administered MDMA to human subjects and measured their oxytocin levels.
They identified ten qualifying studies containing a total of 39 effect size estimates. The original studies used varying doses of MDMA, ranging from 75 to 150 milligrams. The researchers also measured oxytocin from blood or urine samples at different time intervals.
The team analyzed this pooled data, looking specifically at three modifying variables. They tested whether the amount of the drug, the time of measurement, or the sex of the participants altered the amount of oxytocin released.
Time emerged as a modifying factor, showing a curvilinear relationship with hormone levels. After a person took MDMA, their oxytocin levels rose steadily. The levels reached their highest point between 150 and 200 minutes after administration.
Following this peak, oxytocin concentrations began to decline. Some studies noted that levels remained slightly elevated above their baseline even five hours after the drug was taken.
The analysis did not find a statistically significant relationship between the dose of MDMA and the resulting oxytocin levels. The varied dosing strategies used in the original ten studies might explain this lack of an effect. Some studies gave all participants a flat dose, while others adjusted the amount based on a person’s body weight.
The team also found a slight trend regarding the sex of the participants. The results suggested that studies with a higher proportion of female subjects tended to record smaller increases in oxytocin. However, this finding was not statistically significant and requires more targeted testing to confirm.
Readers should exercise caution when interpreting blood or urine oxytocin levels as a direct reflection of brain activity. Oxytocin in the bloodstream does not easily cross the blood-brain barrier, meaning peripheral levels might not perfectly mirror the amounts acting directly on brain circuits.
Still, recent physiological studies suggest that circulating oxytocin can influence the brain indirectly. The hormone can stimulate the vagus nerve, a major neural pathway connecting the body’s internal organs to the brainstem. This vagal pathway might carry the social and emotional signals generated by peripheral oxytocin into the central nervous system.
The meta-analysis also revealed a high degree of unexplained variance among the ten studies. The statistical models showed that differences in time, dose, and sex only accounted for about a quarter of the variation in the results. This indicates that other unmeasured biological factors are influencing how much oxytocin the body releases in response to MDMA.
The potential difference in how males and females respond to the drug might be tied to estrogen. Estrogen is known to regulate how sensitive cells are to oxytocin.
Because the analysis relied on existing published data, the research team could not isolate female-only groups or control for the use of hormonal birth control. These missing details leave the exact nature of the sex difference an open question. Differences in body mass index or the menstrual cycle could potentially alter how a person reacts to the drug.
Methodological differences in how the original researchers processed their biological samples might also have skewed the overall numbers. Oxytocin levels can appear vastly different depending on whether researchers use advanced extraction techniques to isolate the hormone from blood plasma.
Moving forward, scientists need to standardize how they administer MDMA and measure oxytocin. Implementing consistent dosing based on body weight and utilizing uniform extraction methods will yield more reliable data.
The researchers also noted evidence of publication bias in the available literature. Small studies with larger margins of error tended to report disproportionately high oxytocin effects. Conducting studies with a large sample size will help correct this imbalance and verify the true strength of the drug’s impact on the hormonal system.
The study, “The effect of MDMA administration on oxytocin concentration levels: systematic review and a multilevel meta-analysis in humans,” was authored by Anna Vaslavski, Anna Harwood-Gross, Salomon Israel, and Leehe Peled-Avron.
URL: https://www.psypost.org/meta-analysis-confirms-mdma-triggers-sustained-oxytocin-release/
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #MDMA #Oxytocin #PTSDtherapy #Neuroscience #MentalHealthResearch #SocialChemistry #PsychedelicTherapy #OxytocinPeak #ClinicalTrials #MetaAnalysis
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DATE: August 20, 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: New study tracks oxytocin spikes in MDMA therapy trials
URL: https://www.psypost.org/meta-analysis-confirms-mdma-triggers-sustained-oxytocin-release/
The psychoactive drug MDMA temporarily increases levels of the social hormone oxytocin in human subjects, with levels peaking a few hours after use. These findings might help researchers time therapeutic interventions during clinical trials for psychiatric conditions like post-traumatic stress disorder. The research was published in Neuroscience and Biobehavioral Reviews.
The drug 3,4-methylenedioxymethamphetamine, commonly known as MDMA, is classified as an entactogen. This designates it as a psychoactive substance that heavily alters emotional processing. People who take the substance often report enhanced feelings of closeness, empathy, and social unity.
In recent years, MDMA has become the subject of clinical trials for treating post-traumatic stress disorder, commonly called PTSD. Therapists suggest that the drug helps patients build an emotional bond with their doctors. It reduces anxiety related to social interactions and helps people process perceived emotional threats.
Researchers suspect a primary biological mechanism behind these prosocial effects is the release of oxytocin. Oxytocin is a chemical messenger produced in the hypothalamus, a region deep within the brain. It acts as both a local brain signaling molecule and a hormone that circulates throughout the body.
The hormone is best known for its role in childbirth and lactation, but it also regulates social behaviors. Elevated levels of oxytocin are linked to increased empathy, generosity, and trust, particularly among people within the same social group.
MDMA initiates its effects by causing the brain to release a flood of monoamines. These are chemical messengers that include serotonin, dopamine, and norepinephrine.
The sudden surge of serotonin activates specific receptors on neurons in the hypothalamus. Animal models demonstrate that this receptor activation directly triggers the release of oxytocin into the bloodstream and central nervous system.
Medical professionals have tried administering oxytocin directly via nasal sprays to treat social anxiety and similar conditions. However, the nasal spray has a very short active period in the bloodstream, disappearing in just a few minutes.
MDMA, by contrast, has a much longer active window. It promotes a robust release of the body’s own naturally produced oxytocin. This creates a sustained social effect that is better suited for long psychotherapy sessions.
While individual studies have shown that MDMA triggers the release of oxytocin, results have varied widely. Lead author Anna Vaslavski, a researcher at Bar-Ilan University, and her colleagues noticed a gap in the literature. No previous research had systematically gathered and analyzed these disparate studies to figure out exactly how the drug influences oxytocin levels across different times, doses, and demographic groups.
To find answers, the research team conducted a meta-analysis. This is a statistical technique that pools data from multiple independent studies to identify overall trends. The team searched academic databases to find peer-reviewed studies that administered MDMA to human subjects and measured their oxytocin levels.
They identified ten qualifying studies containing a total of 39 effect size estimates. The original studies used varying doses of MDMA, ranging from 75 to 150 milligrams. The researchers also measured oxytocin from blood or urine samples at different time intervals.
The team analyzed this pooled data, looking specifically at three modifying variables. They tested whether the amount of the drug, the time of measurement, or the sex of the participants altered the amount of oxytocin released.
Time emerged as a modifying factor, showing a curvilinear relationship with hormone levels. After a person took MDMA, their oxytocin levels rose steadily. The levels reached their highest point between 150 and 200 minutes after administration.
Following this peak, oxytocin concentrations began to decline. Some studies noted that levels remained slightly elevated above their baseline even five hours after the drug was taken.
The analysis did not find a statistically significant relationship between the dose of MDMA and the resulting oxytocin levels. The varied dosing strategies used in the original ten studies might explain this lack of an effect. Some studies gave all participants a flat dose, while others adjusted the amount based on a person’s body weight.
The team also found a slight trend regarding the sex of the participants. The results suggested that studies with a higher proportion of female subjects tended to record smaller increases in oxytocin. However, this finding was not statistically significant and requires more targeted testing to confirm.
Readers should exercise caution when interpreting blood or urine oxytocin levels as a direct reflection of brain activity. Oxytocin in the bloodstream does not easily cross the blood-brain barrier, meaning peripheral levels might not perfectly mirror the amounts acting directly on brain circuits.
Still, recent physiological studies suggest that circulating oxytocin can influence the brain indirectly. The hormone can stimulate the vagus nerve, a major neural pathway connecting the body’s internal organs to the brainstem. This vagal pathway might carry the social and emotional signals generated by peripheral oxytocin into the central nervous system.
The meta-analysis also revealed a high degree of unexplained variance among the ten studies. The statistical models showed that differences in time, dose, and sex only accounted for about a quarter of the variation in the results. This indicates that other unmeasured biological factors are influencing how much oxytocin the body releases in response to MDMA.
The potential difference in how males and females respond to the drug might be tied to estrogen. Estrogen is known to regulate how sensitive cells are to oxytocin.
Because the analysis relied on existing published data, the research team could not isolate female-only groups or control for the use of hormonal birth control. These missing details leave the exact nature of the sex difference an open question. Differences in body mass index or the menstrual cycle could potentially alter how a person reacts to the drug.
Methodological differences in how the original researchers processed their biological samples might also have skewed the overall numbers. Oxytocin levels can appear vastly different depending on whether researchers use advanced extraction techniques to isolate the hormone from blood plasma.
Moving forward, scientists need to standardize how they administer MDMA and measure oxytocin. Implementing consistent dosing based on body weight and utilizing uniform extraction methods will yield more reliable data.
The researchers also noted evidence of publication bias in the available literature. Small studies with larger margins of error tended to report disproportionately high oxytocin effects. Conducting studies with a large sample size will help correct this imbalance and verify the true strength of the drug’s impact on the hormonal system.
The study, “The effect of MDMA administration on oxytocin concentration levels: systematic review and a multilevel meta-analysis in humans,” was authored by Anna Vaslavski, Anna Harwood-Gross, Salomon Israel, and Leehe Peled-Avron.
URL: https://www.psypost.org/meta-analysis-confirms-mdma-triggers-sustained-oxytocin-release/
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #MDMA #Oxytocin #PTSDtherapy #Neuroscience #MentalHealthResearch #SocialChemistry #PsychedelicTherapy #OxytocinPeak #ClinicalTrials #MetaAnalysis
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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/
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#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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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/
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
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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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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/
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#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
-
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/
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#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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Psychedelics: A Rush Towards Regulatory Acceptance
Government is making it faster to approve new psychedelic drugs for depression, PTSD, and addiction. Find out how this helps patients.
#PsychedelicTherapy, #MentalHealth, #DrugApproval, #FDA, #NewTreatments
https://newsletter.tf/psychedelic-drug-rules-speed-approval-mental-health/