#brainimmuneinteraction — Public Fediverse posts
Live and recent posts from across the Fediverse tagged #brainimmuneinteraction, aggregated by home.social.
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DATE: August 31, 2026 at 10:00AM
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: Stress hormones drive female-specific brain rewiring following ketamine anesthesia
A recent study found that female mice, but not males, experience a surge in a stress hormone during recovery from ketamine anesthesia, prompting immune cells in the brain to reshape neuronal connections. This points to profound sex differences in how the brain regains function after being anesthetized. The findings were published in Science Advances.
Recovery from anesthesia is a complex biological process required to resume normal bodily and brain functions. Ketamine is unique among anesthetics because it targets specific inhibitory systems in the brain. It is normally viewed as a standard anesthetic that causes a temporary and fully reversible loss of consciousness.
Recent observations suggest ketamine can actually reinstate juvenile-like plasticity, or the brain’s ability to rewire and form new connections, and induce mild anxiety in female animals. This aligns with other work showing that biological sex plays a role in anesthesia responses. For instance, a study covered by PsyPost in 2024 indicated that females tend to regain consciousness and cognitive function faster than males following exposure to general anesthetics.
Microglia, the resident immune cells of the brain, are known to interact with neuronal networks and respond to environmental changes, shaping how neurons fire. However, their specific role in anesthesia recovery, particularly regarding potential sex differences, has remained largely unexplored.
The research, led by Alessandro Venturino and Sandra Siegert, a professor at the Institute of Science and Technology Austria, aimed to see if microglia behave differently in male and female brains during anesthesia recovery.
“We were interested to investigate which consequences ketamine anesthesia had on microglia,” said Siegert, who leads the Siegert Group. “Microglia are known to respond to neuronal activity and anesthesia alters the brain activity, which led us to hypothesize that microglia might respond to it.”
To test this, the team administered a single dose of a ketamine-based anesthesia mixture to adult male and female mice. They then examined the primary visual cortex, an area of the brain where ketamine is known to induce structural changes.
Looking at the brain tissue four hours after the injection, the scientists noticed a distinct difference between the sexes. Female mice exhibited increased levels of a protein called CD68 in their microglia, indicating heightened cellular activity. The physical shape of the female microglia also changed, and they formed prolonged contacts with the branching structures of nearby neurons. Male microglia did not show these pronounced changes.
To see if these cellular contacts altered brain function, the team recorded the electrical activity of the neurons in slices of brain tissue. They found that the frequency of spontaneous electrical impulses increased in the female mice, suggesting enhanced neural plasticity and synaptic function. When the researchers chemically depleted the microglia in a separate group of female mice before administering the anesthesia, this boost in electrical activity did not occur. This provides evidence that the immune cells are necessary for the observed neural changes.
The researchers then used genetic sequencing to figure out what was driving this female-specific response. They found that female microglia selectively increased the expression of a gene called Fkbp5. This gene produces a protein involved in the body’s response to stress hormones, particularly corticosterone.
Blood tests confirmed that two hours after the ketamine injection, female mice had corticosterone levels nearly three times higher than their baseline. In contrast, male corticosterone levels remained relatively flat. To test the role of this hormone, the team surgically removed the adrenal glands, which produce corticosterone, in a group of female mice.
Without the adrenal glands, the ketamine-induced changes in microglial activity and neuron interaction vanished. When these mice were given a direct injection of corticosterone, the microglia rapidly resumed their active state and began contacting neurons again. This indicates that the stress hormone directly drives the immune cells to remodel neural connections.
The findings are in line with research covered by PsyPost in 2026, which detailed how recovering from ketamine anesthesia triggers a female-specific surge in corticosterone that activates microglia to promote new neural connections.
“It was fascinating to see that not the typical suspicious candidates for sex differences, namely the sex hormone estrogen, is the main driver of this effect but that the effect is mediated through the stress-response via the hormone corticosterone,” Siegert said.
A general reader might assume these findings mean human women will experience identical brain remodeling after receiving ketamine. The authors note that the study was conducted in mice, and human biological responses to anesthetics and stress hormones can differ. The experimental design also focused on a single time point of four hours post-anesthesia, meaning the long-term persistence of these new neural connections is currently unknown.
The anesthetic dosage used in the experiment also differs from how the drug is sometimes applied in psychiatry. The researchers gave the animals a dose sufficient to reach a level of anesthesia deep enough to perform surgery without pain or movement. “It’s important to say that we used an anesthetic dosage of ketamine, in combination with other drugs commonly used to ensure surgical plane for animal surgery,” Siegert noted. “How much our results can be translated to dosages commonly used for treating depression requires a follow-up study.”
Despite these caveats, the results highlight how biological sex can fundamentally alter the body’s response to pharmacological treatments. “Medication can have different effects and consequences between sexes,” Siegert explained. “In the case of ketamine, we know surprisingly little about sex-differences, even though it is frequently used. Our data suggests that females are more sensitive to the effects of ketamine.”
Beyond hormones, other factors such as the neurotransmitter noradrenaline appear to fluctuate differently between the sexes during recovery and might interact with the stress response. Future research could explore how different types of anesthetics, which act on different brain receptors, might influence these immune-driven changes.
More broadly, the team hopes to continue unraveling the mysteries of these immune cells and how they interact with glial cells, the supportive, non-neuronal cells that protect and maintain the brain. “Our main research focus is on identifying which role microglia have in the adult healthy brain,” Siegert said. “They are highly active but we still have only a rudimentary understanding of their daily role on how they act on neurons and other glial cells in the brain.”
The study, “Corticosterone-linked microglial activity underpins sexually dimorphic neuroplasticity after ketamine anesthesia,” was authored by Alessandro Venturino, MohammadAmin Alamalhoda, Thomas Negrello, Kelly Jin, Cindy T. J. van Velthoven, Ryan John A. Cubero, Jake Yeung, Peter Koppensteiner, Bosiljka Tasic, and Sandra Siegert.
-------------------------------------------------
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 #KetamineRecovery #MicrogliaSexDifferences #CorticosteroneStressResponse #SexDifferencesInNeuroscience #NeuroplasticityAfterAnesthesia #FemaleBrainsOnly #NeuralRewiring #CorticosteroneDrivenPlasticity #BrainImmuneInteraction #KetamineResearch
-
DATE: August 31, 2026 at 10:00AM
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: Stress hormones drive female-specific brain rewiring following ketamine anesthesia
A recent study found that female mice, but not males, experience a surge in a stress hormone during recovery from ketamine anesthesia, prompting immune cells in the brain to reshape neuronal connections. This points to profound sex differences in how the brain regains function after being anesthetized. The findings were published in Science Advances.
Recovery from anesthesia is a complex biological process required to resume normal bodily and brain functions. Ketamine is unique among anesthetics because it targets specific inhibitory systems in the brain. It is normally viewed as a standard anesthetic that causes a temporary and fully reversible loss of consciousness.
Recent observations suggest ketamine can actually reinstate juvenile-like plasticity, or the brain’s ability to rewire and form new connections, and induce mild anxiety in female animals. This aligns with other work showing that biological sex plays a role in anesthesia responses. For instance, a study covered by PsyPost in 2024 indicated that females tend to regain consciousness and cognitive function faster than males following exposure to general anesthetics.
Microglia, the resident immune cells of the brain, are known to interact with neuronal networks and respond to environmental changes, shaping how neurons fire. However, their specific role in anesthesia recovery, particularly regarding potential sex differences, has remained largely unexplored.
The research, led by Alessandro Venturino and Sandra Siegert, a professor at the Institute of Science and Technology Austria, aimed to see if microglia behave differently in male and female brains during anesthesia recovery.
“We were interested to investigate which consequences ketamine anesthesia had on microglia,” said Siegert, who leads the Siegert Group. “Microglia are known to respond to neuronal activity and anesthesia alters the brain activity, which led us to hypothesize that microglia might respond to it.”
To test this, the team administered a single dose of a ketamine-based anesthesia mixture to adult male and female mice. They then examined the primary visual cortex, an area of the brain where ketamine is known to induce structural changes.
Looking at the brain tissue four hours after the injection, the scientists noticed a distinct difference between the sexes. Female mice exhibited increased levels of a protein called CD68 in their microglia, indicating heightened cellular activity. The physical shape of the female microglia also changed, and they formed prolonged contacts with the branching structures of nearby neurons. Male microglia did not show these pronounced changes.
To see if these cellular contacts altered brain function, the team recorded the electrical activity of the neurons in slices of brain tissue. They found that the frequency of spontaneous electrical impulses increased in the female mice, suggesting enhanced neural plasticity and synaptic function. When the researchers chemically depleted the microglia in a separate group of female mice before administering the anesthesia, this boost in electrical activity did not occur. This provides evidence that the immune cells are necessary for the observed neural changes.
The researchers then used genetic sequencing to figure out what was driving this female-specific response. They found that female microglia selectively increased the expression of a gene called Fkbp5. This gene produces a protein involved in the body’s response to stress hormones, particularly corticosterone.
Blood tests confirmed that two hours after the ketamine injection, female mice had corticosterone levels nearly three times higher than their baseline. In contrast, male corticosterone levels remained relatively flat. To test the role of this hormone, the team surgically removed the adrenal glands, which produce corticosterone, in a group of female mice.
Without the adrenal glands, the ketamine-induced changes in microglial activity and neuron interaction vanished. When these mice were given a direct injection of corticosterone, the microglia rapidly resumed their active state and began contacting neurons again. This indicates that the stress hormone directly drives the immune cells to remodel neural connections.
The findings are in line with research covered by PsyPost in 2026, which detailed how recovering from ketamine anesthesia triggers a female-specific surge in corticosterone that activates microglia to promote new neural connections.
“It was fascinating to see that not the typical suspicious candidates for sex differences, namely the sex hormone estrogen, is the main driver of this effect but that the effect is mediated through the stress-response via the hormone corticosterone,” Siegert said.
A general reader might assume these findings mean human women will experience identical brain remodeling after receiving ketamine. The authors note that the study was conducted in mice, and human biological responses to anesthetics and stress hormones can differ. The experimental design also focused on a single time point of four hours post-anesthesia, meaning the long-term persistence of these new neural connections is currently unknown.
The anesthetic dosage used in the experiment also differs from how the drug is sometimes applied in psychiatry. The researchers gave the animals a dose sufficient to reach a level of anesthesia deep enough to perform surgery without pain or movement. “It’s important to say that we used an anesthetic dosage of ketamine, in combination with other drugs commonly used to ensure surgical plane for animal surgery,” Siegert noted. “How much our results can be translated to dosages commonly used for treating depression requires a follow-up study.”
Despite these caveats, the results highlight how biological sex can fundamentally alter the body’s response to pharmacological treatments. “Medication can have different effects and consequences between sexes,” Siegert explained. “In the case of ketamine, we know surprisingly little about sex-differences, even though it is frequently used. Our data suggests that females are more sensitive to the effects of ketamine.”
Beyond hormones, other factors such as the neurotransmitter noradrenaline appear to fluctuate differently between the sexes during recovery and might interact with the stress response. Future research could explore how different types of anesthetics, which act on different brain receptors, might influence these immune-driven changes.
More broadly, the team hopes to continue unraveling the mysteries of these immune cells and how they interact with glial cells, the supportive, non-neuronal cells that protect and maintain the brain. “Our main research focus is on identifying which role microglia have in the adult healthy brain,” Siegert said. “They are highly active but we still have only a rudimentary understanding of their daily role on how they act on neurons and other glial cells in the brain.”
The study, “Corticosterone-linked microglial activity underpins sexually dimorphic neuroplasticity after ketamine anesthesia,” was authored by Alessandro Venturino, MohammadAmin Alamalhoda, Thomas Negrello, Kelly Jin, Cindy T. J. van Velthoven, Ryan John A. Cubero, Jake Yeung, Peter Koppensteiner, Bosiljka Tasic, and Sandra Siegert.
-------------------------------------------------
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 #KetamineRecovery #MicrogliaSexDifferences #CorticosteroneStressResponse #SexDifferencesInNeuroscience #NeuroplasticityAfterAnesthesia #FemaleBrainsOnly #NeuralRewiring #CorticosteroneDrivenPlasticity #BrainImmuneInteraction #KetamineResearch
-
DATE: August 31, 2026 at 10:00AM
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: Stress hormones drive female-specific brain rewiring following ketamine anesthesia
A recent study found that female mice, but not males, experience a surge in a stress hormone during recovery from ketamine anesthesia, prompting immune cells in the brain to reshape neuronal connections. This points to profound sex differences in how the brain regains function after being anesthetized. The findings were published in Science Advances.
Recovery from anesthesia is a complex biological process required to resume normal bodily and brain functions. Ketamine is unique among anesthetics because it targets specific inhibitory systems in the brain. It is normally viewed as a standard anesthetic that causes a temporary and fully reversible loss of consciousness.
Recent observations suggest ketamine can actually reinstate juvenile-like plasticity, or the brain’s ability to rewire and form new connections, and induce mild anxiety in female animals. This aligns with other work showing that biological sex plays a role in anesthesia responses. For instance, a study covered by PsyPost in 2024 indicated that females tend to regain consciousness and cognitive function faster than males following exposure to general anesthetics.
Microglia, the resident immune cells of the brain, are known to interact with neuronal networks and respond to environmental changes, shaping how neurons fire. However, their specific role in anesthesia recovery, particularly regarding potential sex differences, has remained largely unexplored.
The research, led by Alessandro Venturino and Sandra Siegert, a professor at the Institute of Science and Technology Austria, aimed to see if microglia behave differently in male and female brains during anesthesia recovery.
“We were interested to investigate which consequences ketamine anesthesia had on microglia,” said Siegert, who leads the Siegert Group. “Microglia are known to respond to neuronal activity and anesthesia alters the brain activity, which led us to hypothesize that microglia might respond to it.”
To test this, the team administered a single dose of a ketamine-based anesthesia mixture to adult male and female mice. They then examined the primary visual cortex, an area of the brain where ketamine is known to induce structural changes.
Looking at the brain tissue four hours after the injection, the scientists noticed a distinct difference between the sexes. Female mice exhibited increased levels of a protein called CD68 in their microglia, indicating heightened cellular activity. The physical shape of the female microglia also changed, and they formed prolonged contacts with the branching structures of nearby neurons. Male microglia did not show these pronounced changes.
To see if these cellular contacts altered brain function, the team recorded the electrical activity of the neurons in slices of brain tissue. They found that the frequency of spontaneous electrical impulses increased in the female mice, suggesting enhanced neural plasticity and synaptic function. When the researchers chemically depleted the microglia in a separate group of female mice before administering the anesthesia, this boost in electrical activity did not occur. This provides evidence that the immune cells are necessary for the observed neural changes.
The researchers then used genetic sequencing to figure out what was driving this female-specific response. They found that female microglia selectively increased the expression of a gene called Fkbp5. This gene produces a protein involved in the body’s response to stress hormones, particularly corticosterone.
Blood tests confirmed that two hours after the ketamine injection, female mice had corticosterone levels nearly three times higher than their baseline. In contrast, male corticosterone levels remained relatively flat. To test the role of this hormone, the team surgically removed the adrenal glands, which produce corticosterone, in a group of female mice.
Without the adrenal glands, the ketamine-induced changes in microglial activity and neuron interaction vanished. When these mice were given a direct injection of corticosterone, the microglia rapidly resumed their active state and began contacting neurons again. This indicates that the stress hormone directly drives the immune cells to remodel neural connections.
The findings are in line with research covered by PsyPost in 2026, which detailed how recovering from ketamine anesthesia triggers a female-specific surge in corticosterone that activates microglia to promote new neural connections.
“It was fascinating to see that not the typical suspicious candidates for sex differences, namely the sex hormone estrogen, is the main driver of this effect but that the effect is mediated through the stress-response via the hormone corticosterone,” Siegert said.
A general reader might assume these findings mean human women will experience identical brain remodeling after receiving ketamine. The authors note that the study was conducted in mice, and human biological responses to anesthetics and stress hormones can differ. The experimental design also focused on a single time point of four hours post-anesthesia, meaning the long-term persistence of these new neural connections is currently unknown.
The anesthetic dosage used in the experiment also differs from how the drug is sometimes applied in psychiatry. The researchers gave the animals a dose sufficient to reach a level of anesthesia deep enough to perform surgery without pain or movement. “It’s important to say that we used an anesthetic dosage of ketamine, in combination with other drugs commonly used to ensure surgical plane for animal surgery,” Siegert noted. “How much our results can be translated to dosages commonly used for treating depression requires a follow-up study.”
Despite these caveats, the results highlight how biological sex can fundamentally alter the body’s response to pharmacological treatments. “Medication can have different effects and consequences between sexes,” Siegert explained. “In the case of ketamine, we know surprisingly little about sex-differences, even though it is frequently used. Our data suggests that females are more sensitive to the effects of ketamine.”
Beyond hormones, other factors such as the neurotransmitter noradrenaline appear to fluctuate differently between the sexes during recovery and might interact with the stress response. Future research could explore how different types of anesthetics, which act on different brain receptors, might influence these immune-driven changes.
More broadly, the team hopes to continue unraveling the mysteries of these immune cells and how they interact with glial cells, the supportive, non-neuronal cells that protect and maintain the brain. “Our main research focus is on identifying which role microglia have in the adult healthy brain,” Siegert said. “They are highly active but we still have only a rudimentary understanding of their daily role on how they act on neurons and other glial cells in the brain.”
The study, “Corticosterone-linked microglial activity underpins sexually dimorphic neuroplasticity after ketamine anesthesia,” was authored by Alessandro Venturino, MohammadAmin Alamalhoda, Thomas Negrello, Kelly Jin, Cindy T. J. van Velthoven, Ryan John A. Cubero, Jake Yeung, Peter Koppensteiner, Bosiljka Tasic, and Sandra Siegert.
-------------------------------------------------
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 #KetamineRecovery #MicrogliaSexDifferences #CorticosteroneStressResponse #SexDifferencesInNeuroscience #NeuroplasticityAfterAnesthesia #FemaleBrainsOnly #NeuralRewiring #CorticosteroneDrivenPlasticity #BrainImmuneInteraction #KetamineResearch
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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/
-------------------------------------------------
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 #PsychedelicsAndImmuneHealth #DOIPrevention #5HT2AReceptor #Neuroinflammation #HippocampusProtection #LPSInflammation #Cytokines #NeuropsychiatricResearch #MiceStudy #BrainImmuneInteraction
-
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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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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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
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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