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(https://www.psypost.org/mitochondria-appear-to-play-key-role-in-link-between-positive-experiences-and-brain-health/) Mitochondria appear to play key role in link between positive experiences and brain health
Jul 24th 2024, 10:00

A new study by researchers at Columbia University sheds light on how our experiences and emotions might influence brain health. The study provides evidence that mitochondria, the tiny powerhouses inside our brain cells, could be the key players in this relationship. In older adults, positive psychosocial experiences — such as a larger social network or a greater sense of purpose — are linked to healthier brain mitochondria. Conversely, negative experiences — like social isolation or depression — are associated with less robust mitochondrial function.
The findings have been published in the (https://www.pnas.org/doi/10.1073/pnas.2317673121) Proceedings of the National Academy of Sciences (PNAS).
“How the mind shapes our biology, potential for health, and risk of disease is perhaps the biggest gap in medicine. We know from decades of research, and from our personal experiences, that how we feel influences our health. But there is little science on this,” said study author (https://www.picardlab.org/) Martin Picard, an associate professor and endowed chair in energy and health.
“Mitochondria are the energy and information processor of each cell. They keep us alive and well, and enable each cells in our body and brain to communicate with each other and to act as an integrated whole – to be in health. We need to uncover the psychobiological connections linking what we experience to the biology of energy. This is the focus of mitochondrial psychobiology, and of this study by Dr. Caroline Trumpff.”
To better understand the role of mitochondria, the researchers used data from two long-term studies involving nearly 450 older adults in the United States. These participants had provided detailed information about their psychosocial experiences over two decades and had agreed to donate their brains for postmortem analysis.
The researchers aimed to quantify both positive and negative psychosocial experiences. They created indices that combined various psychosocial factors into overall positive and negative scores. Positive factors included a larger social network, greater social activity, a strong sense of purpose, and overall well-being.
Negative factors encompassed social isolation, depressive symptoms, negative mood, and perceived stress. By converting these reports into standardized scores, the researchers could systematically compare the participants’ psychosocial experiences with the biological state of their brain mitochondria.
For the biological analysis, the researchers focused on the dorsolateral prefrontal cortex, a brain region involved in executive functions and emotional regulation. They measured the abundance of mitochondrial proteins in this area using sophisticated proteomic techniques. Instead of analyzing thousands of individual mitochondrial genes, they grouped related genes into seven categories, or “mitotypes,” which reflect different aspects of mitochondrial function. This innovative approach allowed for a more interpretable and statistically robust analysis of mitochondrial health.
The findings revealed a clear association between psychosocial experiences and mitochondrial protein abundance. Participants with higher positive psychosocial scores had greater levels of mitochondrial proteins, particularly those involved in oxidative phosphorylation (OxPhos), a key process for cellular energy production. In contrast, those with higher negative psychosocial scores had lower levels of these proteins.
“We’re showing that older individuals’ state of mind is linked to the biology of their brain mitochondria, which is the first time that subjective psychosocial experiences have been related to brain biology,” explained Trumpff, an assistant professor of medical psychology.
“In our lives we are exposed to positive and negative psychosocial factors, some of which we can nourish and develop,” Picard told PsyPost. “These factors, we now learn in Dr. Trumpff’s study, are linked to the biology of the energy transformation centers in our brains – the mitochondria. We have long known that things like exercise, fasting, and low carb diets can stimulate mitochondria. This study brings subjective experiences – that stuff that makes us human – in the mix of things that may influence energy flow in our brains.”
A key finding of the study was that psychosocial experiences accounted for 18 to 25% of the variance in the abundance of complex I proteins. Complex I is the largest and most upstream enzyme in the OxPhos pathway. This significant percentage indicates that a considerable portion of the differences in mitochondrial function among individuals can be attributed to their psychosocial experiences. Positive psychosocial factors were linked to higher levels of proteins involved in energy transformation, while negative factors were associated with lower levels of these proteins.
The researchers were surprised by the strength of the effects. “The psycho-biological correlation of 18-25% is remarkable compared to other similar studies,” Picard said.
Interestingly, the findings also suggested that glial cells and neurons might respond to or even contribute to psychosocial experiences in opposite ways. Glial cells, which include astrocytes, microglia, and oligodendrocytes, were found to have higher mitochondrial gene expression associated with positive psychosocial experiences. This means that individuals who reported more positive experiences had glial cells with more active mitochondrial functions.
In contrast, the same positive experiences were linked to lower mitochondrial gene expression in neurons. This divergence indicates that while glial cells might enhance their energy production and other mitochondrial functions in response to positive experiences, neurons might reduce these activities.
Glial cells play supportive roles in the brain, such as providing nutrients to neurons, maintaining homeostasis, and participating in immune responses. Their increased mitochondrial activity in response to positive experiences could enhance these supportive functions, potentially leading to better overall brain health. On the other hand, neurons, which are primarily responsible for transmitting information throughout the brain, might reduce mitochondrial activity as a way to optimize energy use or reduce oxidative stress under positive psychosocial conditions.
These results were consistent across various subgroups, including different genders and cognitive statuses, indicating a broad and robust connection between psychosocial experiences and mitochondrial health. But as with all research, there are some caveats to consider. One major limitation is the reliance on postmortem brain samples.
“We obviously had to ask people how they felt before they died, and had to wait for them to die to analyze their mitochondria postmortem,” Picard noted. “So there is a time gap between the psychosocial assessment and the biological measures.”
Developing non-invasive techniques to measure mitochondrial health in living individuals could significantly advance this field of research. Such methods would enable continuous monitoring of mitochondrial function, allowing for early detection of potential issues and timely interventions. Researchers are already exploring ways to assess mitochondrial health in clinical settings, which could revolutionize how we monitor and promote brain health.
“Our long-term goals are to create a science of health and healing that integrates the science of energy with the human experience of energy,” Picard said. “This will help us bring the mind into medicine, and create a more holistic framework to help each person reach their optimal state of health.”
The study, “(https://doi.org/10.1073/pnas.2317673121) Psychosocial experiences are associated with human brain mitochondrial biology,” was authored by Caroline Trumpff, Anna S. Monzel, Carmen Sandi, Vilas Menon, Hans-Ulrich Klein, Masashi Fujita, Annie Lee, Vladislav A. Petyuk, Cheyenne Hurst, Duc M. Duong, Nicholas T. Seyfried, Aliza P. Wingo, Thomas S. Wingo, Yanling Wang, Madhav Thambisetty, Luigi Ferrucci, David A. Bennett, Philip L. De Jager, and Martin Picard.

(https://www.psypost.org/african-elephants-address-one-another-by-name-study-finds/) African elephants address one another by name, study finds
Jul 24th 2024, 08:00

A recent study published in (https://doi.org/10.1038/s41559-024-02420-w) Nature Ecology & Evolution has uncovered that wild African elephants communicate with individually specific calls, akin to human names. This groundbreaking discovery suggests that elephants use unique sound patterns to refer to each other, without imitating the vocalizations of the addressed individual. Researchers developed a statistical model that could identify the intended recipient of an elephant’s call with 20% accuracy, significantly better than random chance.
One of the hallmarks of human language is the use of names. Humans use specific sets of sounds to refer to specific objects or individuals. When a human baby is born, its caregivers decide on a set of sounds or letters to refer to the newborn throughout its lifetime. This is called a name.
An important feature of human names is that they are arbitrary in structure. If a newborn baby is named Mary, John, or any other name, that specific set of sounds or letters forming the name has no connection with any of the baby’s features. Others cannot infer a person’s name just by observing them (unless they observe the person saying their own name) because the name has nothing to do with the person’s characteristics. The only way we can learn another person’s name is if someone tells us or if we read it somewhere. Similarly, if a person changes their name, others can use the new name without any issues.
But it has been unclear if there are any species aside from humans that can use names like this. Previous studies found that species like bottlenose dolphins and some parrots refer to other members of their species by imitating the sounds that particular individual makes. However, this severely limits the possible complexity of the communication.
Study author Michael A. Pardo and his colleagues analyzed contact and greeting rumbles from female-offspring groups of wild African savannah elephants to determine whether they might contain vocal labels similar to the names humans use for each other. They recorded a set of 527 calls of elephants from the greater Samburu ecosystem in northern Kenya and 98 calls from Amboseli National Park in southern Kenya, identifying both the elephant sending the call (the sender) and the elephant it was addressed to (the receiver, the elephant who responded to the call).
These calls came from 114 different elephants as the callers and 119 different elephants as receivers. For 597 of these calls, both the caller and the receiver belonged to the same family group.
“The most common call type produced by elephants is the rumble, a harmonically rich, low-frequency sound that is individually distinct, distinguishable, and produced across most behavioral contexts. Contact rumbles are long-distance calls produced when the caller is visually separated from one or more social affiliates and attempting to reinitiate contact. Greeting rumbles are close-distance calls produced when one individual approaches another after a period of separation,” the study authors explain.
The authors conducted statistical analyses of these calls and determined that they are specific to individual receivers. In other words, it was possible to determine with some accuracy from the sounds contained in the call who the receiver was. This indicates that elephants use specific sound combinations as vocal labels for specific elephants. They address other elephants by name.
The authors created a statistical model that predicted the identity of the elephant a call was directed to with 20% accuracy. While far from perfect, this accuracy is much better than random guessing, confirming that the calls of these elephants contain combinations of sounds that refer to specific other elephants. Further statistical analysis indicated that the calls indeed refer to individual elephants and do not depend on the relatedness or age of the elephants in question.
In humans, different people address the same individual by the same name. The study authors wanted to test whether this is the case with elephants as well, but the evidence was inconclusive. The statistical machine learning model was not able to predict better than chance who a specific elephant was addressing if the model was not trained on calls of the sender elephant. Thus, it remains unknown whether elephants use the same name for the same individual or if different elephants use different names for the same elephant (kind of like different people addressing us using different nicknames).
Finally, the authors played recorded calls to 17 wild elephants and found that they reacted much more strongly to playbacks of calls addressed to them than to calls addressed to other elephants.
“To our knowledge, this study presents the first evidence for vocal addressing of conspecifics [other members of the same species] without imitation of the receiver’s calls in nonhuman animals. Very few species are known to address conspecifics with vocal labels of any kind. Where evidence for vocal labels has been found, they are either clearly imitative or of unknown structure. Our data suggest that elephants label conspecifics without relying on imitation of the receiver’s calls, a phenomenon previously known to occur only in human language.”, study authors concluded.
The study makes an important contribution to the scientific understanding of social interactions in elephants. However, it should be noted that the ability of the statistical model developed in the study to identify receivers of calls was far from perfect, likely indicating that individual names (vocal labels) are not used in every call and that more research is needed before elephant calls are fully understood.
The paper, “(https://www.nature.com/articles/s41559-024-02420-w) African elephants address one another with individually specific name-like calls,” was authored by Michael A. Pardo, Kurt Fristrup, David S. Lolchuragi, Joyce H. Poole, Petter Granli, Cynthia Moss, Iain Douglas-Hamilton, and George Wittemyer.

(https://www.psypost.org/autistic-traits-may-protect-against-loot-box-overspending-study-suggests/) Autistic traits may protect against loot box overspending, study suggests
Jul 24th 2024, 06:00

Video gaming has become a global phenomenon, with over 2.46 billion players worldwide in 2022 contributing to a staggering $347 billion in revenue. A significant portion of this revenue comes from microtransactions — small in-game purchases that enhance the gaming experience. Among these, loot boxes, which offer random virtual items, have sparked considerable debate due to their similarity to gambling.
A recent study published in (https://doi.org/10.1038/s41598-024-64812-z) Scientific Reports explored whether gamers with autistic traits are more susceptible to excessive gaming and problematic gambling behaviors, and their spending patterns on loot boxes. Surprisingly, the study found that while gamers with higher levels of autistic traits may be more vulnerable to excessive gaming and problematic gambling, they actually spend less on loot boxes when their gambling symptoms are accounted for.
“Video gaming as a hobby has evolved substantially over the years, with how people access and play video games shifting along with technological advancements. Research into this increasingly popular hobby has grown in response,” said study author James D. Sauer of the University of Tasmania.
“One such change in the gaming industry includes the rise of the microtransaction monetization model. This allows games companies to accrue revenue from their product by offering additional, optional, in-game purchases. ‘Loot boxes’ are a particular type of microtransaction that has become prevalent within video games, and has received considerable attention from game users and researchers alike.”
“Loot boxes have been demonstrated to be structurally, psychologically, and legally akin to gambling,” Sauer explained. “As such, researchers have become interested in understanding if some game users may be more vulnerable to over-engagement with, or over-expenditure on these optional, virtual items.”
“Presently there is little scientific understanding about how individual differences are associated with spending on microtransaction features. Neurodevelopmental differences, such as autism and ADHD, have previously been reported to be linked to problematic engagement with video games, however, there is less research into the relationship between neurodivergence and microtransaction expenditure.”
For their study, the researchers recruited 1,178 participants through Prolific Academic, an online research platform. The participants were adults from Australia, Aotearoa (New Zealand), and the United States, ensuring a diverse but primarily Western sample. Participants were required to be at least 18 years old.
The researchers utilized several validated scales to measure different aspects of gaming behaviors, gambling symptoms, and autistic traits. The Internet Gaming Disorder Checklist (IGD), a nine-item scale, assessed problematic gaming behaviors with items like “I have lost interest in other hobbies or entertainment in order to play games” and “I feel irritable, anxious or sad when I am unable to game.”
The Problem Gambling Severity Index (PGSI), another nine-item scale, measured the severity of problematic gambling symptoms over the past year with items such as “Have you bet more than you could really afford to lose?” and “Has gambling caused you any health problems, including stress or anxiety?” The Risky Loot Box Index, a five-item scale, evaluated risky engagement with loot boxes through statements like “The thrill of opening loot boxes has encouraged me to buy more” and “I frequently play games longer than I intend to, so I can earn loot boxes.”
The Ritvo Autism and Asperger Diagnostic Scale (RAADS-14), a 14-item self-report questionnaire, screened for autistic traits in adults with items like “It is difficult for me to understand how other people are feeling when we are talking.” Participants also reported their spending on loot boxes and non-randomized microtransactions in the past month. The data was converted to U.S. dollars for consistency.
The researchers found strong positive correlations between problematic gaming behaviors, problematic gambling symptoms, risky loot box engagement, and spending on both loot boxes and non-randomized microtransactions. This indicates that individuals who exhibit more problematic gaming and gambling behaviors are also more likely to spend money on these in-game features. These findings align with previous research demonstrating that those with higher levels of problematic behaviors tend to spend more on microtransactions.
Interestingly, the study found that participants with higher levels of autistic traits reported higher levels of problematic gaming behaviors, problematic gambling symptoms, and risky loot box engagement. However, the strength of these associations was generally weak.
Contrary to the researchers’ initial predictions, there was no evidence that individuals with higher levels of autistic traits spent more on loot boxes or non-randomized microtransactions. In fact, when gambling symptoms were statistically controlled for, higher levels of autistic traits were associated with lower spending on loot boxes. “Thus, characteristics and experiences of autism may be slightly protective of overspending on loot boxes,” Sauer told PsyPost.
Moderation analyses further supported these findings. Autistic traits did not significantly influence the relationship between problematic gaming and gambling behaviors and spending on microtransactions. However, a consistent pattern emerged showing that higher levels of autistic traits were associated with reduced spending on loot boxes.
This nuanced result highlights that while individuals with autistic traits may be more vulnerable to problematic behaviors, they might also be more cautious or deliberate in their spending decisions, particularly concerning loot boxes.
“Previous research has consistently found that higher levels of problematic gaming and problematic gambling is associated with higher levels of loot box expenditure, and as such, it was surprising to us that our data showed that gamers higher in autistic characteristics and experiences, who we found to be higher in problematic gaming and gambling symptomatology, are not also reporting higher loot box expenditure,” Sauer remarked. “That’s what’s great about research, it’s not about what you believe, it’s about what the empirical evidence shows!”
However, it is important to note that the study did not screen for clinically diagnosed autism, meaning the sample included individuals with varying levels of autistic traits but not necessarily those with a formal diagnosis. This could affect the applicability of the results to clinically diagnosed populations.
Furthermore, the study’s cross-sectional design prevents causal conclusions. While the data indicate a relationship between autistic traits and gaming behaviors, it is unclear whether these traits cause changes in gaming behavior or if other unmeasured variables are at play. Longitudinal studies are needed to better understand these relationships over time.
“We do not know whether experiencing higher levels of autistic traits causes game users to engage with video games in a problematic way, or to spend less on loot boxes or if some unmeasured variable is causing this relationship,” Sauer explained. “We can say that our data indicates a relationship between these factors, but that this is not the complete picture. Further research is required to better understand the relationship between neurodivergence and video gaming behaviors.”
“Ultimately, we want to better understand how microtransaction models, and particularly those with gambling-like features, affect those who play video games. The more science can help us understand, hopefully the more game consumers can know about the products they engage with, and make more informed decisions for themselves and their children.”
The study, “(https://www.nature.com/articles/s41598-024-64812-z) The associations between autistic characteristics and microtransaction spending,” was authored by Tegan Charnock, Aaron Drummond, Lauren C. Hall, and James D. Sauer.

(https://www.psypost.org/new-neuroscience-research-cbd-does-not-temper-thcs-effects-on-brain-connectivity-may-enhance-disruption/) New neuroscience research: CBD does not temper THC’s effects on brain connectivity, may enhance disruption
Jul 23rd 2024, 16:00

In a recent study published in the journal (https://doi.org/10.1038/s41386-024-01891-6) Neuropsychopharmacology, researchers have found that cannabidiol (CBD) does not mitigate the disruptive effects of delta-9-tetrahydrocannabinol (THC) on brain connectivity. In fact, the study suggests that CBD might even exacerbate these effects in some cases. This challenges the commonly held belief that CBD can counterbalance the psychoactive impact of THC in cannabis.
The research was motivated by the growing use of cannabis among adolescents and young adults, a period characterized by significant brain development. Previous studies indicated that chronic cannabis use during adolescence could lead to changes in brain connectivity and cognitive impairments. However, there was a lack of detailed research on the acute effects of cannabis in this age group, especially considering the different compositions of cannabis with varying levels of THC and CBD.
THC is the main psychoactive component, responsible for the euphoric “high” and cognitive alterations associated with cannabis use. CBD, on the other hand, is non-psychoactive and has been suggested to have potential therapeutic properties, such as reducing anxiety and possessing anti-inflammatory effects. While THC binds directly to cannabinoid receptors in the brain, influencing mood, perception, and cognition, CBD interacts more subtly with these receptors and can modulate the effects of THC.
The study was conducted as part of the larger “CannTeen” project and involved 48 semi-regular cannabis users. The participants were evenly divided into two groups: 24 adolescents with a mean age of 17.2 years and 24 adults with a mean age of 27.8 years. The selection criteria ensured that participants had used cannabis between 0.5 and 3 days per week over the past three months. The researchers aimed to match the cannabis use frequency between the adolescent and adult groups.
Participants were recruited from the Greater London area through various means, including school assemblies, physical posters, flyers, and online advertisements. Before each of the three sessions, participants were screened for recent drug and alcohol use through saliva and breathalyser tests to ensure no recent consumption.
The study used a double-blind, placebo-controlled design. Each participant underwent three drug administration sessions where they inhaled one of three types of cannabis: placebo (0 mg THC, 0 mg CBD), THC-only (8 mg THC for a 75 kg person, zero CBD), or THC + CBD (8 mg THC and 24 mg CBD for a 75 kg person).
The cannabis was administered using a Volcano Medic Vaporizer to ensure precise dosing and controlled administration. The participants then underwent a resting-state functional magnetic resonance imaging (fMRI) scan approximately 50 minutes after inhalation to capture the peak effects of the drugs.
Resting-state fMRI is a technique used to measure and map brain activity by detecting changes associated with blood flow. This method involves scanning the brain while the participant is not performing any specific tasks, allowing researchers to observe the natural fluctuations in brain activity and connectivity between different regions.
The study’s findings revealed significant disruptions in brain connectivity across several key networks after cannabis administration. These networks include the executive control network (ECN), salience network, hippocampal network, and limbic striatal network.
Specifically, the ECN, responsible for higher-order cognitive functions like decision-making and cognitive control, showed reduced connectivity under the influence of both THC and THC + CBD. The salience network, which helps in detecting and filtering important stimuli, also displayed diminished connectivity.
The hippocampal network, essential for memory formation and retrieval, was similarly affected. Furthermore, the limbic striatal network, involved in reward processing and emotion regulation, experienced connectivity reductions.
One of the most striking findings was that the addition of CBD did not mitigate the disruptive effects of THC on brain connectivity. In fact, in some cases, the presence of CBD led to even greater reductions in connectivity than THC alone, particularly in the ECN and salience networks. This challenges the widely held belief that CBD can counterbalance the psychoactive effects of THC.
“This study has shown that acute cannabis administration reduces connectivity within resting-state networks and between brain regions associated with cognition and emotional processing,” the researchers concluded. “Contrary to some previous work, CBD does not appear to have any attenuating effects when combined with THC, and in some networks, the addition of CBD further reduced network connectivity. This may be due to the metabolic competition of CBD and THC leading to higher plasma THC when CBD is also present.”
“There were no interaction effects between age group and drug treatments suggesting that adolescents do not show differential effects of cannabis compared to adults. These results therefore suggest that cannabis containing high levels of CBD may not necessarily be safer for users and that adolescent cannabis users appear to be at no greater risk than young adults with acute cannabis use, however further research is required to assess the long-term effects of cannabis, particularly past young adulthood.”
The study, “(https://www.nature.com/articles/s41386-024-01891-6) Acute effects of different types of cannabis on young adult and adolescent resting-state brain networks,” was authored by Natalie Ertl, Tom P. Freeman, Claire Mokrysz, Shelan Ofori, Anna Borissova, Kat Petrilli, H. Valerie Curran, Will Lawn, and Matthew B. Wall.

(https://www.psypost.org/psilocybin-reduces-alcohol-use-by-altering-gene-expression-in-brains-reward-center/) Psilocybin reduces alcohol use by altering gene expression in brain’s reward center
Jul 23rd 2024, 14:00

New research has found that psilocybin reduces alcohol consumption in rats by altering specific brain pathways, particularly in the left nucleus accumbens. This suggests that psilocybin could potentially be a useful treatment for reducing alcohol use, but more research is needed to confirm its effectiveness in humans. The study has been published in the journal (https://doi.org/10.1093/brain/awae136) Brain.
Alcohol use disorder is a chronic condition characterized by an inability to control or stop drinking despite adverse social, occupational, or health consequences. This disorder ranges in severity and can lead to significant disability and increased mortality. Traditional treatments include behavioral therapy, medication, and support groups, but many people struggle to achieve lasting recovery, highlighting the need for more effective therapeutic options.
Psilocybin is a naturally occurring psychedelic compound found in certain species of mushrooms. It has been used for centuries in various cultural and spiritual contexts. In recent years, scientific interest in psilocybin has resurged due to its potential therapeutic benefits. When ingested, psilocybin is converted into psilocin, a compound that interacts with serotonin receptors in the brain, influencing mood, perception, and cognition.
Early clinical trials suggest that psilocybin-assisted therapy may be effective in treating various mental health conditions, including depression, anxiety, and substance use disorders. Preliminary research has also shown that psilocybin may help reduce alcohol consumption, but the exact mechanisms remain unclear. The new study aimed to explore the neurobiological effects of psilocybin, particularly focusing on its interaction with serotonin and dopamine receptors in the brain’s reward circuit.
The study was conducted using 66 male Long-Evans rats, which were chosen based on their suitability for modeling human alcohol consumption behaviors. They were housed individually under a controlled light/dark cycle and had unlimited access to food and water. The study followed strict ethical guidelines for the care and use of laboratory animals.
Initially, the rats were given access to a 20% ethanol solution in a two-bottle choice setup for four weeks to establish ethanol consumption. Following this period, the rats were trained to self-administer ethanol in operant cages, a method that involves pressing a lever to receive a dose of ethanol. This setup mimics human voluntary alcohol consumption and allows researchers to measure the rats’ motivation to consume alcohol.
The study was divided into several experiments to isolate different variables. In one experiment, psilocybin was injected intraperitoneally (directly into the body cavity) at a dose of 1 mg/kg. Another experiment involved microinfusing psilocybin directly into the left or right nucleus accumbens, a key brain region involved in reward processing. These injections aimed to identify specific brain areas responsible for psilocybin’s effects on alcohol consumption.
To understand the molecular effects, the researchers measured the expression of various genes in the nucleus accumbens and prefrontal cortex four hours after psilocybin administration. This analysis focused on genes related to serotonin and dopamine pathways, which are crucial in regulating reward and addiction behaviors.
The researchers found that psilocybin induced significant changes in gene expression in the nucleus accumbens. Notably, the genes coding for serotonin receptors and dopamine transporters showed differential expression between the left and right nucleus accumbens. For instance, the gene for the serotonin receptor 2A (5-HT2A) was downregulated in the left nucleus accumbens, while brain-derived neurotrophic factor (BDNF) was upregulated in the right nucleus accumbens.
Psilocybin administration led to a notable reduction in alcohol self-administration. Rats that received psilocybin showed a 48% decrease in the number of lever presses and a 51% reduction in total alcohol intake compared to those receiving a saline solution. This suggests that psilocybin’s effects are robust and not limited to direct brain infusions.
Interestingly, when psilocybin was microinjected into the left nucleus accumbens, the number of lever presses for alcohol decreased by 38%, and the total alcohol intake dropped by 39%. In contrast, injections into the right nucleus accumbens did not produce significant changes, highlighting the importance of the left nucleus accumbens in mediating these effects.
The involvement of serotonin receptors was confirmed when the effects of psilocybin were blocked by pre-treatment with ketanserin, a serotonin receptor antagonist. Rats receiving ketanserin before psilocybin did not show the usual reduction in alcohol consumption, indicating that psilocybin’s effects are mediated through serotonin receptor pathways.
The study provides evidence that psilocybin can reduce alcohol consumption in rats through its action on specific brain pathways. By altering gene expression in the nucleus accumbens and involving serotonin receptors, psilocybin appears to reduce the rewarding properties of alcohol, leading to decreased intake.
While these findings shed light on the potential mechanisms of psilocybin in reducing alcohol consumption, there are significant physiological and behavioral differences between rats and humans that must be accounted for. Consequently, translating these results to human alcohol use disorder treatment will require extensive clinical research to confirm efficacy and safety in human populations.
The study, “(https://academic.oup.com/brain/advance-article-abstract/doi/10.1093/brain/awae136/7664633) Psilocybin reduces alcohol self-administration via selective 1 left nucleus accumbens activation in rats,” was authored by Jérôme Jeanblanc, Romain Bordy, Grégory Fouquet, Virginie Jeanblanc, and Mickaël Naassila.

(https://www.psypost.org/study-finds-r-ketamine-restores-cognitive-deficits-induced-by-chronic-social-isolation/) Study finds (R)-ketamine restores cognitive deficits induced by chronic social isolation
Jul 23rd 2024, 12:00

A recent study on mice found that chronic social isolation reduces the activity of neurons in the anterior insular cortex region of the brain, resulting in impaired social memory. Treatment with (R)-ketamine counteracted this reduction, restoring social memory functioning in these mice. The paper was published in (https://doi.org/10.1038/s41380-024-02419-6) Molecular Psychiatry.
Humans need contact with other humans to stay healthy and maintain their mental well-being. Newborns require human interaction to develop their cognitive abilities adequately. Chronic social isolation occurs when a person has little or no contact with others for prolonged periods. This condition is typically accompanied by feelings of loneliness and disconnection.
Chronic social isolation can have severe mental health effects, including depression and anxiety. It can also result in cognitive decline or impaired cognitive development in children. Physically, it is associated with an increased risk of conditions such as heart disease, weakened immune function, and higher mortality rates. Over time, the lack of social contact can exacerbate stress and lead to a diminished sense of purpose.
The effects of social isolation occur because the brain changes its functioning when a person is exposed to chronic social isolation. Study author Rei Yokoyama and his colleagues aimed to examine whether some of these adverse changes could be counteracted with a pharmaceutical treatment. They focused on ketamine.
Ketamine is a medication primarily used for anesthesia and pain relief, but it is also utilized in lower doses for its rapid-acting antidepressant effects in the treatment of depression and other mental health conditions. It is usually a mixture of two molecular configurations: (R)-ketamine and (S)-ketamine.
(S)-ketamine is generally considered to have greater anesthetic potency and a faster onset of action, while (R)-ketamine has attracted research interest due to its potentially longer-lasting antidepressant effects with fewer side effects. The researchers were particularly interested in (R)-ketamine.
The researchers conducted a study on mice, dividing them into two groups. One group of mice was raised in social isolation, starting from three weeks of age, and kept individually isolated for six weeks in opaque plastic cages. The other group was housed 5-6 per cage in clear plastic cages of the same size.
When the mice were nine weeks old, the researchers began behavioral tests to assess their cognitive functioning. They conducted tests to measure animal analogues of feelings of helplessness (the forced swim test), social interactions (the three-chamber test), and memory (the five-trial social memory test). After these tests, the researchers conducted a series of physiological experiments on the mice.
The results showed that mice reared in social isolation displayed worse cognitive functioning in social memory tests. This impairment was accompanied by unique patterns of reduced neural activity in the anterior insular cortex after social contact. Treatment with (R)-ketamine, but not (S)-ketamine, counteracted this reduction in neural activity, effectively restoring social memory and social cognition in these mice.
“Our findings on the ability of (R)-ketamine to ameliorate social cognitive deficits may contribute to the development of treatments for various mental disorders that share similar social cognitive deficits,” the study authors concluded.
The study demonstrated that the two molecular configurations of ketamine have different effects on mice and that (R)-ketamine can counteract the effects of social isolation. However, this was a study on mice, not humans. While mice and humans share many physiological similarities, they are still very different species. Because of this, the effects on humans might not be identical.
Further research is necessary to explore the potential of (R)-ketamine as a treatment for social cognitive deficits in humans. Clinical trials would be essential to determine its efficacy and safety in treating mental disorders characterized by similar deficits.
The paper, “(https://doi.org/10.1038/s41380-024-02419-6) (R)-ketamine restores anterior insular cortex activity and cognitive deficits in social isolation-reared mice,” was authored by Rei Yokoyama, Yukio Ago, Hisato Igarashi, Momoko Higuchi, Masato Tanuma, Yuto Shimazaki, Takafumi Kawai, Kaoru Seiriki, Misuzu Hayashida, Shun Yamaguchi, Hirokazu Tanaka, Takanobu Nakazawa, Yasushi Okamura, Kenji Hashimoto, Atsushi Kasai, and Hitoshi Hashimoto.

Forwarded by:
Michael Reeder LCPC
Baltimore, MD

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