#brainplasticity — Public Fediverse posts
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DATE: August 13, 2026 at 06:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Single dose of rapamycin rapidly reduces autism-like traits in adult mice
URL: https://www.psypost.org/single-dose-of-rapamycin-rapidly-reduces-autism-like-traits-in-adult-mice/
A new study published in the journal Nature Communications suggests that exposing mice to mild inflammation during pregnancy triggers brain and behavioral changes in their offspring that resemble autism spectrum disorder. The research provides evidence that a single dose of the immunosuppressive drug rapamycin can rapidly but temporarily reverse these symptoms in adult mice by altering brain function rather than physical structure.
Autism spectrum disorder is a complex condition associated with diverse changes in brain development, behavior, and sensory processing. One known risk factor is maternal immune activation, which occurs when a pregnant mother experiences an infection or inflammation. This inflammatory response can alter the development of the fetal brain. In both human and animal studies, such early immune events are linked to later neurodevelopmental differences, including increased brain volume in early life, altered social behaviors, and heightened sensitivity to sensory input.
At the cellular level, many of these changes are associated with the overactivation of the mTOR pathway. The mTOR pathway is a biological signaling network that regulates cell growth, division, and survival. When this system is hyperactive, it tends to lead to abnormal synapse formation, an imbalance between excitatory and inhibitory brain signals, and an increased susceptibility to seizures.
“We have a longstanding interest in the mTOR system in brain development and autism spectrum disorder,” said study authors Harley Kornblum, director of the UCLA Intellectual and Developmental Disabilities Research Center and a professor of psychiatry, pediatrics, and pharmacology; Neil Harris, a professor of neurosurgery; and Janel Le Belle, an associate professor of neurosurgery. “Our earlier study also led by Dr. Le Belle showed that mild maternal inflammation in a strain of mouse activated the mTOR system and resulted in many behaviors reminiscent of autism and that are also found in genetic mouse models in which we know that the affected genes cause autism in people.”
Rapamycin is an established drug that inhibits the mTOR pathway. It is commonly used in medicine to prevent organ transplant rejection. In previous animal research, treating young mice with rapamycin over several weeks prevented the physical brain abnormalities associated with certain genetic mutations linked to autism.
“We were interested in trying treatment with the mTOR inhibitor rapamycin, which is used in children with disorders that activate the mTOR pathway,” the researchers added. However, chronic use of rapamycin can suppress the immune system and inhibit healthy growth. The authors designed this study to observe what happens when adult mice receive a short-acting, single dose of the drug, focusing on immediate functional changes in the brain rather than long-term structural remodeling.
The authors triggered a mild maternal inflammatory response in pregnant mice by injecting them with lipopolysaccharide, a bacterial compound that induces an immune reaction. This low dose was designed to provoke a response without making the pregnant mice noticeably ill. The offspring were then raised to early adulthood or older adulthood, creating experimental groups of male and female mice to compare against a control group that received a harmless saline solution.
The researchers first evaluated the physical and molecular characteristics of the offspring exposed to maternal inflammation. They tracked brain weights from birth to 200 days old for 16 mice per group. The exposed mice experienced mild brain overgrowth early in life compared to the control group, but by day 200, this growth had slowed, resulting in brain weights slightly below the control average.
The exposed mice also maintained chronically elevated levels of immune proteins, known as cytokines, in their blood. Their brain tissue showed persistent overactivation of the mTOR pathway. To see if immune cells were driving the ongoing issues, the researchers depleted microglia, a type of brain immune cell, in some mice. This reduction improved behaviors in young adult mice but failed to help older adult mice, suggesting that other functional mechanisms maintain the behavioral traits later in life.
To test behavior, the scientists observed groups of 26 mice in open field tests. The exposed mice spent roughly twice as much time engaging in repetitive behaviors, such as grooming and circling, compared to the control mice. When the researchers administered a single injection of rapamycin at a dose of 5 milligrams per kilogram, the repetitive behaviors in the exposed mice dropped to match the levels seen in the control mice within two hours.
“We were very surprised by the rapidity of the effects of rapamycin,” the researchers told PsyPost. “We expected that if the mTOR system was still activated in the adult, it would be influencing the structure of how brain cells connect with each other, which would mean that anticipated effects would take longer than just a few hours.”
This behavioral rescue was temporary, as the repetitive behaviors returned to their previous elevated levels 72 hours later. The authors also tested daily injections over five weeks in groups of 10 mice. They found that the mice developed a tolerance to the drug, leading to a gradual loss of its behavioral benefits.
The study also measured sensory over-responsivity, a common trait where individuals are highly sensitive to touch or sound. Using groups of eight mice, the researchers tested tactile avoidance by placing the animals in a box with both smooth and rough floor surfaces. The exposed mice actively avoided the rough-textured floor, spending less time there than the control mice. Following a single dose of rapamycin, the exposed mice increased their time spent on the rough floor, indicating a normalization of their sensory tolerance.
Sensory sensitivities can disrupt daily life and exacerbate other challenges. “Our results point to a significant role of the sensory system in our mouse model and its correction with rapamycin,” the authors noted. “Sensory symptoms are known to be highly disabling in autism and now there is some evidence that abnormalities in sensory responsiveness may contribute to many of the behaviors that we don’t normally view as being mediated by the sensory system.”
Because sensory and behavioral changes often relate to how brain cells fire, the researchers examined the electrical activity of individual brain cells. They analyzed brain slices from 24 mice per group, focusing on pyramidal neurons in the sensory cortex. The neurons from the exposed mice exhibited a higher frequency and amplitude of spontaneous electrical discharges compared to the control neurons, indicating hyper-excitability. Treating the mice or the brain slices with rapamycin quickly reduced this hyperactivity.
To test this hyper-excitability in living animals, the researchers administered a seizure-inducing chemical to groups of eight mice. All eight exposed mice experienced visible seizures at a high dose, compared to only two out of eight control mice. Rapamycin administration lowered the severity of the seizure scores in the exposed group.
To observe brain-wide communication, the authors used functional magnetic resonance imaging to scan 16 mice per group. This technique measures functional connectivity, which tracks how different brain regions synchronize their activity. The exposed mice displayed higher levels of connectivity than the control mice, particularly between sensory processing areas and subcortical regions like the thalamus. Following the two-hour rapamycin treatment, this hyper-connectivity decreased in the sensory cortex and reorganized across the brain, restoring the functional network to a state that closely resembled the control mice.
This neural reorganization provides evidence that specific circuits remain adaptable in adult mice. The average person should take away the idea “[t]hat some behaviors associated with autism can improve, even after the brain has matured,” the authors said. “Furthermore, we have identified the pathways (connections) in the brain that are influenced in this mouse model and that are altered with rapamycin.”
Finally, the researchers analyzed gene expression in the brain cells. They found that the exposed mice had altered activity in genes related to ion channels, which control the flow of electrical charges in and out of cells. After the acute rapamycin treatment, the expression of genes associated with brain cell excitability and autism risk quickly shifted back toward typical levels. This indicates that the drug works by rapidly adjusting the molecular balance of excitation and inhibition.
The findings from this study rely on a specific animal model of maternal inflammation, and physiological responses seen in mice do not directly translate to human neurodevelopment. Because rapamycin has strong immunosuppressive properties, it is not a practical daily treatment for behavioral or sensory symptoms in humans.
“We don’t believe that rapamycin or its close relatives that are currently used clinically will be the ‘cure’ for autism,” the authors cautioned. “First, our effects were temporary and wore off after several treatments. Second, as a class of medications, they can have significant side effects, especially immunosuppression.” They emphasized that they “would not recommend treatment with these medications outside of the conditions for which they are approved.”
Instead of acting as a direct treatment, the drug helps reveal underlying mechanisms for scientists to target. “We look at our findings as a fulcrum to further study autism-associated behaviors and symptoms and how they can be treated,” the authors explained.
Moving forward, the research team plans to explore other interventions. “In one set of studies we are trying to discover the downstream molecular pathways by which rapamycin acts so that we can potentially develop new therapies,” they said. “In the other approach, we are investigating the neural pathways that are misregulated in our model to see if these pathways can be functionally manipulated by therapeutic means, such as transcranial magnetic stimulation.”
The study, “Acute rapamycin treatment reveals distinct mechanisms of dysfunction in a maternal inflammation mouse model,” was authored by JE Le Belle, M. C. Condro, C. Cepeda, KD Oikonomou, K. Tessema, L. Dudley, J. Schoenfield, R. Kawaguchi, D. Geschwind, AJ Silva, Z. Zhang, K. Shokat, NG Harris, and HI Kornblum.
URL: https://www.psypost.org/single-dose-of-rapamycin-rapidly-reduces-autism-like-traits-in-adult-mice/
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #AutismResearch #Rapamycin #mTOR #MaternalInflammation #Neuroscience #BrainPlasticity #AutismTherapies #Neurodevelopment #SensoryProcessing #NeuralConnectivity
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DATE: August 12, 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: Newly engineered psychedelic shows therapeutic promise without gastrointestinal distress
A recent study published in Science Signaling provides evidence that a newly engineered psychedelic compound can produce antidepressant and anti-anxiety effects in mice without causing gastrointestinal side effects. By altering the chemical structure of an existing psychedelic drug, researchers created a variant that targets specific brain receptors linked to mental health benefits but avoids receptors associated with nausea and physical discomfort.
“Psychedelics such as psilocybin and LSD are showing therapeutic potential for individuals with severe psychiatric conditions, including depression, anxiety and PTSD,” explained study co-authors Javier González-Maeso, a professor of pharmacology and toxicology at the Virginia Commonwealth University School of Medicine, and Malgorzata Dukat, a professor of medicinal chemistry at the Virginia Commonwealth University School of Pharmacy. “However, like most therapeutic drugs, psychedelics can also produce unwanted side effects.”
“Another interesting aspect of this field is that essentially all psychedelics currently being studied clinically belong to three major chemical classes: phenethylamines, such as mescaline; tryptamines, such as psilocybin; and ergolines, such as LSD,” the authors noted. “Despite their chemical differences, many of their hallucinogenic and potentially therapeutic effects are mediated through the serotonin 2A receptor (or 5-HT2A receptor) in the brain, as first proposed by Prof. Richard A. Glennon (coauthor of the manuscript) in 1984.”
The serotonin 2A receptor mediates positive mood and neural adaptability, but the drugs that target it often lack specificity. “We became interested in quipazine, a serotonergic compound first described in the 1960s and originally investigated as a potential antidepressant,” the authors explained. “Quipazine was never developed for routine medical use, in part because it also activates another serotonin receptor, the 5-HT3 receptor, which is highly expressed in the gastrointestinal system and can produce significant gastrointestinal side effects.”
To separate the therapeutic benefits from adverse physical reactions, the authors sought to chemically redesign quipazine. “Our goal was to combine medicinal chemistry in Dr. Dukat’s laboratory with molecular and behavioral pharmacology in Dr. Maeso’s laboratory to design, synthesize and test new compounds derived from quipazine,” the researchers said.
“The Dukat team had already investigated 5-HT2 and 5-HT3 structure-activity relationships and found that quinazolines bind at, but are devoid of, 5-HT3 receptor activation,” the authors told PsyPost. “We wanted compounds that retained activity at the 5-HT2A receptor while minimizing activity at the 5-HT3 receptor; hence, investigation of quipazine/quinazoline hybrid molecules. That effort led us to design VCU-1012, a novel quinazoline compound that activates the 5-HT2A receptor while showing minimal activity at the 5-HT3 receptor.”
The authors synthesized several variations of the quipazine molecule and tested these new compounds on human embryonic kidney cells. When the scientists screened VCU-1012 against a panel of over 40 other receptors, it showed minimal off-target activity. VCU-1012 completely failed to activate the serotonin 3 receptor, indicating it might bypass the physical distress seen with the original drug.
This broad testing approach relied on multiple areas of scientific specialty. “This study was a highly collaborative effort,” González-Maeso and Dukat noted. “It brought together the medicinal chemistry expertise of Dr. Dukat’s laboratory and the molecular and behavioral pharmacology expertise of the Maeso laboratory, along with important contributions from other teams at VCU. These included the laboratory of Scott Ramsey, which helped characterize effects at the 5-HT3 receptor; the laboratory of Imad Damaj, which contributed expertise in mouse behavioral models, and the laboratory of Hamid Akbarali, which evaluated gastrointestinal motility.”
To test the physical side effects in a living organism, the researchers evaluated gastrointestinal function in male mice, using six to eight animals per group. They fed the mice a harmless charcoal solution and measured how far the charcoal traveled through the small intestine over a 30-minute period. Mice injected with the original quipazine drug at a dose of 5 milligrams per kilogram of body weight experienced a severe slowdown in digestion. In contrast, mice given VCU-1012 at 1 milligram per kilogram showed normal intestinal movement that was indistinguishable from mice given a plain saline vehicle injection.
Next, the team evaluated behavioral effects by measuring a specific head-twitch behavior in groups of six mice. This rapid side-to-side head movement is a standard animal proxy for hallucinogenic effects. VCU-1012 prompted a robust increase in head twitches within the first 15 minutes of administration, which was completely blocked when mice were pretreated with a drug that selectively prevents serotonin 2A receptor activation.
To evaluate potential antidepressant properties, the researchers used a forced-swim test. Mice were placed in a beaker of water for a short time to induce a passive coping state, which is characterized by floating rather than swimming. Twenty-four hours after receiving VCU-1012, the classical psychedelic psilocybin, or a saline vehicle, the mice were retested. The researchers also performed this test on a separate group of eight to ten genetically modified mice lacking the serotonin 2A receptor.
Both psilocybin and VCU-1012 reduced floating time in normal mice, which suggests an antidepressant-like effect lasting well beyond the drug’s immediate hallucinogenic window. In the genetically modified mice lacking the serotonin 2A receptor, VCU-1012 had no behavioral effect. Psilocybin still reduced floating time in the modified mice, which indicates psilocybin relies on additional biological pathways that VCU-1012 does not engage.
The researchers also explored whether the compound could alleviate anxiety caused by medical treatments. They repeatedly administered the chemotherapy drug paclitaxel to groups of seven or eight mice to induce a prolonged state of anxiety. Anxiety was measured by observing how much time the mice spent in the brightly lit section of a specialized testing box.
Paclitaxel noticeably reduced the time mice spent in the light area. A single dose of VCU-1012 given 24 hours prior restored normal exploratory behavior, countering the chemotherapy-induced anxiety without altering the animals’ general movement levels.
To understand how the drug alters the brain on a microscopic level, the scientists examined dendritic spines. These are tiny protrusions on the branches of brain cells that help form synapses, or connections, with other neurons. The team used a fluorescent virus to visually highlight neurons in the frontal cortex, analyzing 40 to 106 neurons from three or four mice per group.
Both psilocybin and VCU-1012 increased the density of mature, mushroom-shaped dendritic spines 24 hours after a single dose. This change indicates enhanced brain plasticity and stronger neural connections. Just as in the behavioral tests, this structural brain plasticity did not occur in mice lacking the serotonin 2A receptor.
Finally, the researchers used computer modeling and mutated receptor cells to see exactly how VCU-1012 fits into the serotonin 2A receptor. “One particularly interesting finding came from examining how VCU-1012 interacts with the 5-HT2A receptor,” the authors observed. “You can think of the receptor’s binding pocket as a small three-dimensional lock. A drug with the right shape and chemical properties can fit into that lock and change how the receptor behaves.”
“We found that VCU-1012 occupies this binding pocket in a different three-dimensional orientation from serotonin, the neurotransmitter that naturally activates the receptor,” they continued. “That finding suggests that there may be additional ways to chemically engage the 5-HT2A receptor beyond those used by classical psychedelics. This opens new possibilities for designing chemically distinct classes of psychedelic compounds and investigating how different interactions with the same receptor influence their biological and behavioral effects.”
The data suggests that VCU-1012 fits into the receptor’s primary binding pocket in a slightly different orientation than the body’s natural serotonin, relying on a specific network of hydrogen bonds. “Our study shows that it is possible to design a psychedelic-like compound from a new chemical class that produces potentially beneficial behavioral and brain-plasticity effects in mice while avoiding an important receptor associated with gastrointestinal side effects,” the researchers said.
Animal models of anxiety and depression, such as the forced-swim test and the light-dark box, cannot fully capture the complexity of human psychiatric disorders. A mouse’s physical responses do not perfectly translate to the subjective emotional experiences or hallucinogenic trips reported by humans. The therapeutic efficacy observed in these experiments might not completely predict actual clinical outcomes in human patients.
“These findings are preclinical, and VCU-1012 is not ready for use in humans,” the authors noted. “Although we were able to greatly reduce its activity at the 5-HT3 receptor, VCU-1012 still interacts with other receptors, including the 5-HT2B receptor. Activation of this receptor can be associated with peripheral side effects, including cardiac valvulopathy.”
Because cardiac valvulopathy involves damage to the heart’s valves, avoiding this off-target receptor is an important safety consideration. “Therefore, additional medicinal chemistry will be necessary to improve the selectivity and safety profile of this new class of compounds before considering clinical development,” they added. All behavioral and neurological tests in this study were conducted exclusively on male mice. Because biological sex often influences how bodies process drugs, future research will need to include female animals to determine if these effects apply universally.
“One major goal is to conduct additional structure-activity relationship studies to design compounds with greater selectivity for the 5-HT2A receptor and fewer off-target effects,” the authors explained. They also hope to answer fundamental questions about how these drugs work. “A broader question we hope to address is whether the hallucinogenic effects produced by classical psychedelics, and by compounds such as VCU-1012, are necessary for their potentially beneficial effects on behavior and brain plasticity.”
“Understanding whether these properties can be separated could help guide the development of the next generation of psychedelic-inspired therapeutics,” they concluded. “The study illustrates how combining medicinal chemistry, molecular pharmacology and animal models can help us understand how psychedelic drugs work and, ultimately, guide the design of compounds with improved therapeutic and safety profiles.”
The study, “Design of a new psychedelic quipazine analog with therapeutic efficacy and potentially fewer side effects,” was authored by Jason Younkin, Ajay H. Bansode, Somdatta Saha, Archana Paymode, Jessica L. Maltman, Charles B. Jones, Justin M. Silverman, Belle Buzzi, Alaina M. Jaster, Michael Fiorillo, Jeremy Rolquin, George D. Miller, Roya Abedi, Minho Kang, Maya Gaines-Smith, Enrique I. Valenzuela Lesme, Mattias Embretsen, Jennifer T. Wolstenholme, Richard A. Glennon, Hamid I. Akbarali, M. Imad Damaj, I. Scott Ramsey, Małgorzata Dukat, and Javier González-Maeso.
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #psychedelics #VCU1012 #5HT2A #mentalhealthresearch #antidepressant #anxietytherapy #drugdesign #serotoninreceptors #brainplasticity #quipazine
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Study Reveals Brain's Ability to Enhance Multitasking Through Practice
📰 Original title: Your Brain Can Rewire Itself To Allow True Multitasking
🤖 IA: It's clickbait ⚠️
👥 Users: It's clickbait ⚠️View full AI summary https://en.killbait.com/study-reveals-brain-s-ability-to-enhance-multitasking-through-practice.html?utm_source=mastodon_world&utm_medium=social&utm_campaign=killbait.mastodon_world
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DATE: July 24, 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: Learning a new skill triggers both temporary cell swelling and lasting structural growth in the human brain
A new study published in PLoS Biology has found that learning a new motor skill sets off two different types of cellular changes in the human brain. The findings suggest that the brain experiences a temporary swelling of cell bodies followed by a long-lasting growth of cellular extensions in specific regions. This dual response offers a deeper understanding of how the human brain physically adapts when we learn something new.
Neuroplasticity refers to the brain’s ability to remodel its physical structure in response to new experiences. This biological process supports learning and memory, and it also influences a person’s vulnerability to neurological conditions.
Valeria Della-Maggiore, an associate professor at the National University of San Martin and the University of Buenos Aires, led the research. She also serves as an adjunct professor at McGill University and directs the Physiology of Action Lab.
“Structural plasticity, the brain’s ability to remodel its connections in response to experience, is fundamental to learning and memory and shapes development and degenerative disorders,” she told PsyPost. She explained that most human studies over the past two decades have used standard MRI protocols to detect changes in brain microstructure, assuming these changes were always plastic in nature.
“Yet animal studies show that cells may undergo structural changes that do not always reflect synapse remodeling,” Della-Maggiore said. “To disambiguate plastic from non-plastic processes, we combined ultra-high-gradient diffusion MRI with SANDI, a biophysical model that allows making inferences at the level of cellular compartments, that is, cell bodies and cell processes.”
To measure structural changes in humans, scientists have typically relied on a brain scanning technique called diffusion tensor imaging, or DTI. This method measures how water molecules move and diffuse through brain tissue. By tracking this water movement, scientists can infer changes in the brain’s microscopic structure.
DTI blends the signals from various parts of the brain tissue together. “DTI captures a single, global signal: it can tell you that a change in one region lasts longer than in another, but not what underlies it,” Della-Maggiore said. Because of this blending, the technique cannot easily distinguish between a permanent structural change and a temporary biological reaction.
To address this limitation, the authors utilized highly sensitive magnetic resonance imaging paired with the specialized mathematical model called Soma and Neurite Density Imaging, or SANDI. Rather than grouping all tissue signals together, SANDI separates the scanning signals into three distinct categories. These categories include the cell bodies, the cellular extensions called neurites, and the extracellular fluid surrounding the cells.
“This study was only possible through a genuinely multidisciplinary effort, in which neuroscientists, experts in diffusion MRI, mathematicians and modeling specialists, and engineers worked together around a single scientific question,” Della-Maggiore said.
The collaboration included her lab along with the Athinoula A. Martinos Center for Biomedical Imaging at Massachusetts General Hospital, and the Cardiff University Brain Research Imaging Centre. “Bringing these different forms of expertise into alignment is what made it possible to extract biological insight from a non-invasive measurement, something no single discipline could have achieved on its own,” she added.
The study included 29 healthy adults between the ages of 18 and 36, consisting of 16 females and 13 males. All participants were right-handed and reported no history of neurological or psychiatric conditions. They completed a motor sequence learning task involving typing a specific five-number sequence on a keyboard using the four fingers of their left, non-dominant hand. The exact sequence was 4-1-3-2-4, with the number 4 representing the index finger and the number 1 representing the pinky finger.
Participants were instructed to type the sequence as quickly and accurately as possible. They completed 15 practice blocks of this finger-tapping sequence. Each block consisted of 12 sequences and was separated by 25 seconds of rest. The entire training session took about 15 to 20 minutes.
To assess how well the participants retained the skill overnight, they were asked to complete eight additional practice blocks 24 hours later. To track brain activity and physical changes, the scientists used an ultra-high-gradient MRI scanner, which offers exceptional sensitivity for capturing microscopic tissue details. They collected functional MRI scans to measure active brain regions during the task. They also collected advanced diffusion MRI scans at three specific points: before the practice session began, 30 minutes after the practice ended, and 24 hours later.
The behavioral data showed that participants improved their typing speed and accuracy primarily during the short rest periods between practice blocks. The functional brain scans aligned with this observation, revealing increased activity in the brain’s memory and motor regions during these brief breaks. However, the most specific discoveries emerged from the SANDI model used to track cellular changes.
“When you learn a new skill, two processes of different spatial and temporal dynamics take place in your brain at the cellular level,” Della-Maggiore said. “One is transient and occurs at the level of cell bodies, which increase in size across all brain regions engaged by the task. The other is persistent, confined to the regions specifically involved in learning, and occurs at the level of cell processes, compatible with structural plasticity.”
The researchers found that DTI scans alone missed a layer of detail. “Our approach revealed something DTI cannot see, that the regions showing lasting changes also carry a transient response,” Della-Maggiore explained. “In other words, beneath what DTI reads as a single persistent effect, there are in fact two distinct processes unfolding on different timescales.”
Specifically, the researchers found a temporary increase in the apparent density of cell bodies across all the brain areas engaged by the task. These areas included the hippocampus, the primary motor cortex, the posterior parietal cortex, and the precuneus. This physical change was observed 30 minutes after the practice session. By the 24-hour mark, the cell bodies in these regions had returned to their normal baseline size.
“The second [surprise] was the spatial pattern: a transient change at the level of the cell body appeared uniformly across all regions engaged by learning, whereas the sustained change in cellular processes was confined to those regions specific to the learned skill,” Della-Maggiore said. “It was this dissociation, in both space and time, that let us infer different biological processes underlying these responses: a homeostatic process such as swelling of cell bodies induced by increased neuronal activity, and cell-process remodeling mediating genuine structural plasticity.”
The authors propose that this short-lived cell expansion is a temporary biological reaction to balance out intense cellular activity. When brain cells are highly active, they experience an imbalance of ions. To correct this imbalance, water flows into the cells, causing them to temporarily swell.
In addition to the temporary swelling, the SANDI model revealed a second, longer-lasting change in specific areas of the brain. The researchers observed a sustained increase in the density of cellular extensions in the precuneus and the posterior parietal cortex. These cellular extensions include structures like dendrites and axons, which connect different brain cells to one another.
This increase in cellular extensions persisted a full day after the learning task. The researchers noticed a direct link to task performance. “Notably, the more a person improved, the stronger this second change was,” Della-Maggiore said.
Interestingly, this long-lasting structural remodeling did not occur in the hippocampus. The hippocampus is a brain region known for helping encode new memories early in the learning process. The findings suggest that while the hippocampus is engaged initially, the long-term structural changes required to retain a motor skill happen in the outer layers of the brain, known as the cortex.
“The broader message is that a change in brain structure is not, in itself, evidence of learning-related plasticity,” Della-Maggiore said. “Being able to separate these processes in a living brain, non-invasively, provides something that did not exist before in human neuroscience: a mechanistic window onto brain plasticity, allowing us to begin inferring biological mechanisms directly in humans rather than relying on animal models.”
Interpreting these findings requires acknowledging a few limitations related to the scanning technology. The SANDI model estimates relative signal fractions of cell components rather than providing a direct physical measurement of cellular volume. The technique relies on specific mathematical assumptions about how water moves in the brain.
“Our approach does not quantify cells or cell processes directly,” Della-Maggiore explained. “It infers how much different cellular components contribute to the MRI signal, based on a biophysical model whose interpretation is grounded in animal and histological evidence.”
She added that referring to changes in cell bodies or cell processes involves principled inferences, not microscopic observations. “The strength of the method lies in tracking how these signals evolve over time, compared against the person’s own baseline,” she said.
The study focused on a specific finger-tapping task in a small group of healthy young adults. Different types of learning, such as studying a new language or solving complex math problems, might engage different cellular mechanisms. “Our broader aim is to keep refining this approach to probe the biological mechanisms of plasticity in ever greater detail, directly in humans,” Della-Maggiore said.
The researchers hope to apply this multi-compartment imaging approach to other areas of neuroscience. “Beyond learning, distinguishing genuine, adaptive remodeling from other processes could prove valuable in contexts such as development, aging, and disease, including conditions like neurodegeneration or neuroinflammation, where telling apart healthy from harmful structural change is both difficult and clinically important,” she said.
“The results move the field beyond descriptive diffusion changes toward mechanistic inference, which is particularly valuable for studies of learning, development, and disease,” Della-Maggiore concluded.
The study, “Learning engages transient and sustained cellular mechanisms in the human brain,” was authored by Guillermina Griffa, Marco Palombo, Abraham Yeffal, Hong-Hsi Lee, Agustin Solano, Susie Y. Huang, and Valeria Della-Maggiore.
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#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #BrainPlasticity #Neurobiology #LearningAndMemory #Neuroimaging #SANDI #DTI #MotorSkillLearning #DiffusionMRI #Hippocampus #Cortex
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Scientists have been wrong about phantom limbs for decades – new study
#Health #PhantomLimb #Neuroscience #BrainResearch #Brain #Amputation #MedicalStudy #BrainPlasticity #Prosthetics #ChronicPain #NeuroScienceNews #HealthResearch
https://the-14.com/scientists-have-been-wrong-about-phantom-limbs-for-decades-new-study/ -
Epigenetics and Brain Plasticity: The Hidden Forces Behind Our Thoughts
#BrainScience #Neuroscience #Epigenetics #MentalHealth #Genetics #StressResponse #BrainPlasticity #Psychiatry #NeuronalDevelopment #MindAndBody
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How Your Brain Forms Memories: The Role of Long-Term Potentiation
#Neuroscience #BrainPlasticity #Neuroplasticity #LongTermPotentiation #SynapticConnections #Glutamate #Neurotransmitters #CalciumSignaling #GlialCells #CircadianRhythms #BrainHealth #MemoryFormation #Learning #NeuroscienceEducation #BrainScience
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From Neurons to Society: Exploring the Brain’s Role in Empathy and Social Bonds
#SocialNeuroscience #Mindfulness #BrainPlasticity #Empathy #NeuroScience #MentalHealth #Compassion #Neuroplasticity #SocialConnection #SelfGrowth #ScientificDiscovery #HumanConnection
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The Marvel of Auditory and Cognitive Networks Working Together in Your Brain
#AuditoryProcessing #BrainScience #NeuralNetworks #CognitiveScience #Hearing #SpeechRecognition #BrainPlasticity #CentralNervousSystem #SoundProcessing #Neuroscience #ListeningSkills #BrainHealth #AuditoryDisorders #LearningAndMemory
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Nourish Your Mind: The Surprising Connection Between Nutrition and Brain Health
#MentalHealth #BrainHealth #NutritionMatters #Neurogenesis #BrainBoost #Psychobiotics #Antioxidants #NutritionalSupport #BrainPlasticity #HealthyMind #WellnessTips #EatForYourBrain #MindAndBody #Neuroprotection
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A molecule in your brain remembers past signals for seconds — enough to reshape a lifetime of memories. #Neuroscience #MolecularMemory #BrainPlasticity
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Learning new movements doesn't just change brain activity—it rewires the brain's circuits. Discover how UC San Diego scientists uncovered this transformation. #Neuroscience #BrainPlasticity #MotorLearning
https://geekoo.news/learning-rewires-the-brains-motor-pathways/
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Unlock the secrets of how your brain learns. Discover the dynamic changes in synapses that make learning possible. #Neuroscience #BrainPlasticity #UCSDResearch
https://geekoo.news/synaptic-symphony-decoding-the-brains-learning-mechanism/
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The Beautiful Messiness of Being Human: Exploring Emotions, Mind, and Connection
#EmotionalContagion #BrainPlasticity #CognitivePsychology #HumanExperience #Jung #Existentialism #Psychoanalysis #MentalHealth #MindBodyConnection #HumanCondition #Curiosity #Connection #MentalWellness #PersonalGrowth #EmotionalIntelligence
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Newborn neurons in adults may protect against cognitive decline https://www.psypost.org/newborn-neurons-in-adults-may-protect-against-cognitive-decline/?utm_source=dlvr.it&utm_medium=mastodon #Neuroscience #Cognition #MentalHealth #BrainPlasticity #Neurogenesis
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The mind can idle away
Enriching memory stores
Daydreaming pays off -
https://brainpizza.substack.com/p/altered-states-rewiring-cravings
Altered States: Rewiring cravings (Part two) - Semaglutide's potential impact on substance use disorders and brain plasticity
#SemaglutideImpact #BrainPlasticity #SubstanceUseDisorder #AddictionTreatment #HealthResearch #BrainHealth #MedicalAdvancements #HealthcareInnovation #AlteredStatesSeries #HealthAndWellness #Neuroscience #DrugEffects #SUDTreatment #RewiringCravings
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Exercise and the Brain: The Neuroscience of Fitness Explored
Regular exercise profoundly impacts our brain and nervous system.
Exercise stimulates neurogenesis – the creation of new neurons – primarily in the hippocampus, influencing memory and learning while increasing key mood-regulating neurotransmitters. It also enhances brain plasticity, essential for recovery from injury and aging, and improves cognitive functions such as attention and memory.
#Biomedicine #Neuroscience #Brain #Neurology #BrainPlasticity #Neurogenesis #Hippocampus #Learning #Memory #CognitiveFunction #Exercise #Fitness -
Quite happy to share this latest work from our lab. In this study, we have addressed an important question of general importance: if and how brain medications (such as anti-depression drugs) change brain over time. We addressed this by specifically investigating the impact of an important drug, Ketamine.
https://www.biorxiv.org/content/10.1101/2023.04.12.536506v1
#biorxiv #neuroscience #ketamine #brainplasticity
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I wish I remembered my dreams. No, this isn’t a metaphor, though I wish it were! I miss my wild wacky weird dreams.
The dreams stopped a while after my two brain surgeries and four brain radiosurgeries. I survived an unsurvivable cancer — and yay, I’m alive! — but I lost some brain function. Like remembering my dreams. Or tasting chocolate.
Once in awhile I awaken holding a thread to a dream. This gives me hope. I fully believe I’ll get my dream recall back.
