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  1. DATE: August 25, 2026 at 01:06AM
    SOURCE: SCIENCE DAILY PSYCHIATIRY FEED

    TITLE: Depression may shut down the brain’s ability to make new neurons

    URL: sciencedaily.com/releases/2026

    A major study found that adults with depression show disrupted production of new neurons in the hippocampus, potentially weakening the brain’s ability to separate new experiences from painful memories. The researchers also identified broad molecular changes that could open the door to new treatments tailored to different biological forms of depression.

    URL: sciencedaily.com/releases/2026

    -------------------------------------------------

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    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 #DepressionResearch #BrainHealth #Neurogenesis #Hippocampus #MentalHealthAwareness #BiologicalDepression #Neuroscience #NewTreatments #MoodDisorders #MentalHealthScience

  2. DATE: August 25, 2026 at 01:06AM
    SOURCE: SCIENCE DAILY PSYCHIATIRY FEED

    TITLE: Depression may shut down the brain’s ability to make new neurons

    URL: sciencedaily.com/releases/2026

    A major study found that adults with depression show disrupted production of new neurons in the hippocampus, potentially weakening the brain’s ability to separate new experiences from painful memories. The researchers also identified broad molecular changes that could open the door to new treatments tailored to different biological forms of depression.

    URL: sciencedaily.com/releases/2026

    -------------------------------------------------

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    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 #DepressionResearch #BrainHealth #Neurogenesis #Hippocampus #MentalHealthAwareness #BiologicalDepression #Neuroscience #NewTreatments #MoodDisorders #MentalHealthScience

  3. DATE: August 25, 2026 at 01:06AM
    SOURCE: SCIENCE DAILY PSYCHIATIRY FEED

    TITLE: Depression may shut down the brain’s ability to make new neurons

    URL: sciencedaily.com/releases/2026

    A major study found that adults with depression show disrupted production of new neurons in the hippocampus, potentially weakening the brain’s ability to separate new experiences from painful memories. The researchers also identified broad molecular changes that could open the door to new treatments tailored to different biological forms of depression.

    URL: sciencedaily.com/releases/2026

    -------------------------------------------------

    Private, vetted email list for mental health professionals: 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 #DepressionResearch #BrainHealth #Neurogenesis #Hippocampus #MentalHealthAwareness #BiologicalDepression #Neuroscience #NewTreatments #MoodDisorders #MentalHealthScience

  4. DATE: August 25, 2026 at 01:06AM
    SOURCE: SCIENCE DAILY PSYCHOLOGY FEED

    TITLE: Depression may shut down the brain’s ability to make new neurons

    URL: sciencedaily.com/releases/2026

    A major study found that adults with depression show disrupted production of new neurons in the hippocampus, potentially weakening the brain’s ability to separate new experiences from painful memories. The researchers also identified broad molecular changes that could open the door to new treatments tailored to different biological forms of depression.

    URL: sciencedaily.com/releases/2026

    -------------------------------------------------

    Private, vetted email list for mental health professionals: 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 #Depression #BrainHealth #Hippocampus #Neurogenesis #MentalHealthResearch #NeuralPlasticity #BiologicalDepression #NewTreatments #Memories #Neuroscience

  5. DATE: August 25, 2026 at 01:06AM
    SOURCE: SCIENCE DAILY PSYCHOLOGY FEED

    TITLE: Depression may shut down the brain’s ability to make new neurons

    URL: sciencedaily.com/releases/2026

    A major study found that adults with depression show disrupted production of new neurons in the hippocampus, potentially weakening the brain’s ability to separate new experiences from painful memories. The researchers also identified broad molecular changes that could open the door to new treatments tailored to different biological forms of depression.

    URL: sciencedaily.com/releases/2026

    -------------------------------------------------

    Private, vetted email list for mental health professionals: 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 #Depression #BrainHealth #Hippocampus #Neurogenesis #MentalHealthResearch #NeuralPlasticity #BiologicalDepression #NewTreatments #Memories #Neuroscience

  6. DATE: August 25, 2026 at 01:06AM
    SOURCE: SCIENCE DAILY PSYCHOLOGY FEED

    TITLE: Depression may shut down the brain’s ability to make new neurons

    URL: sciencedaily.com/releases/2026

    A major study found that adults with depression show disrupted production of new neurons in the hippocampus, potentially weakening the brain’s ability to separate new experiences from painful memories. The researchers also identified broad molecular changes that could open the door to new treatments tailored to different biological forms of depression.

    URL: sciencedaily.com/releases/2026

    -------------------------------------------------

    Private, vetted email list for mental health professionals: 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 #Depression #BrainHealth #Hippocampus #Neurogenesis #MentalHealthResearch #NeuralPlasticity #BiologicalDepression #NewTreatments #Memories #Neuroscience

  7. DATE: August 25, 2026 at 01:06AM
    SOURCE: SCIENCE DAILY MIND-BRAIN FEED

    TITLE: Depression may shut down the brain’s ability to make new neurons

    URL: sciencedaily.com/releases/2026

    A major study found that adults with depression show disrupted production of new neurons in the hippocampus, potentially weakening the brain’s ability to separate new experiences from painful memories. The researchers also identified broad molecular changes that could open the door to new treatments tailored to different biological forms of depression.

    URL: sciencedaily.com/releases/2026

    -------------------------------------------------

    Private, vetted email list for mental health professionals: 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 #DepressionResearch #Neurogenesis #Hippocampus #BrainHealth #MentalHealthAwareness #DepressionMemories #Neuroscience #BiologicalDepression #NewTreatments #MolecularChanges

  8. DATE: August 25, 2026 at 01:06AM
    SOURCE: SCIENCE DAILY MIND-BRAIN FEED

    TITLE: Depression may shut down the brain’s ability to make new neurons

    URL: sciencedaily.com/releases/2026

    A major study found that adults with depression show disrupted production of new neurons in the hippocampus, potentially weakening the brain’s ability to separate new experiences from painful memories. The researchers also identified broad molecular changes that could open the door to new treatments tailored to different biological forms of depression.

    URL: sciencedaily.com/releases/2026

    -------------------------------------------------

    Private, vetted email list for mental health professionals: 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 #DepressionResearch #Neurogenesis #Hippocampus #BrainHealth #MentalHealthAwareness #DepressionMemories #Neuroscience #BiologicalDepression #NewTreatments #MolecularChanges

  9. DATE: August 25, 2026 at 01:06AM
    SOURCE: SCIENCE DAILY MIND-BRAIN FEED

    TITLE: Depression may shut down the brain’s ability to make new neurons

    URL: sciencedaily.com/releases/2026

    A major study found that adults with depression show disrupted production of new neurons in the hippocampus, potentially weakening the brain’s ability to separate new experiences from painful memories. The researchers also identified broad molecular changes that could open the door to new treatments tailored to different biological forms of depression.

    URL: sciencedaily.com/releases/2026

    -------------------------------------------------

    Private, vetted email list for mental health professionals: 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 #DepressionResearch #Neurogenesis #Hippocampus #BrainHealth #MentalHealthAwareness #DepressionMemories #Neuroscience #BiologicalDepression #NewTreatments #MolecularChanges

  10. DATE: August 25, 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: Neuroscientists map how early-life scent memories evolve and move through the brain

    URL: psypost.org/neuroscientists-ma

    The scent of a particular perfume or a childhood home can often bring back vivid, emotionally charged memories from a person’s earliest years. A recent study on mice suggests that these early-life scent memories are initially stored by specific neurons that develop just after birth, but as time passes and the scent is encountered again, the memory trace relocates to broader networks in the brain. The research, published in PLOS Biology, provides evidence for how the brain encodes, sustains, and eventually reorganizes our most cherished childhood memories.

    Scent-triggered memories are a well-documented psychological phenomenon, famously described by Marcel Proust as a flood of vivid nostalgic feelings brought on by the smell of a madeleine cake. In humans, autobiographical memories linked to scents tend to originate from the first decade of life. These memories also tend to carry a much stronger, more positive emotional tone than memories triggered by sights or sounds.

    Supporting this idea, a 2016 review indicated that scents tied to positive personal memories have a uniquely powerful impact on a person’s mood, often increasing positive emotions and reducing physiological signs of stress. Despite this well-known emotional potency, the exact ways the brain creates and stores these long-lasting scent memories have remained somewhat mysterious.

    When a person or animal smells something, the information first enters the olfactory bulb, a small structure at the front of the brain. Within this structure, specific neurons called granule cells help process the scent. In rodents, a massive wave of these granule cells is born on the very first day of life. Because these neonatal neurons are highly active during childhood and tend to survive for a long time, scientists suspected they might be ideal candidates for storing early-life scent memories.

    Memory researchers also know that the brain’s storage systems do not remain static. According to a framework discussed in a 2018 review, memories often shift between different brain areas as time passes. A memory might initially rely on specific regions, like the hippocampus, before being reorganized and transferred to broader networks in the brain’s outer layers.

    “I have been interested in odor perception and in the mechanisms of brain plasticity underlying olfactory learning since my PhD in Lyon, and later during my postdoctoral research at Cornell University,” said study author Nathalie Mandairon, a director of research at the French National Centre for Scientific Research (CNRS) based at the Lyon Neuroscience Research Center. “This study therefore follows naturally from my previous research.”

    “The question that particularly intrigued me was this: during childhood, we are exposed to a multitude of odors,” Mandairon continued. “Why do some of them remain embedded in our memory for decades, while others disappear? And what brain mechanisms allow these very early olfactory memories to persist or resurface later in life?”

    To find out, the research team began by surveying 647 adults about their earliest scent-based memories. “We found that this memory generally dated back to childhood, before the age of 10,” Mandairon explained. “They were most often associated with a pleasant odor, but also with a particularly positive, sometimes joyful, context.”

    “In most cases, the experience had also been repeated several times during childhood,” she added. “Based on these observations, we developed a mouse model to investigate the brain mechanisms involved in the formation and long-term maintenance of this early olfactory memory.”

    During the mouse equivalent of childhood, the researchers placed the animals in a large, enriched cage filled with toys, tunnels, and opportunities for social interaction. They paired this playful environment with a specific attractive odorant over five separate sessions. Microphones recorded the mice emitting a higher number and frequency of high-pitched squeaks, known as ultrasonic vocalizations, which indicates a positive emotional state.

    When the mice reached young adulthood, at two months of age, the researchers tested their reactions to the childhood odorant. The mice that had experienced the scent in the playful environment spent more time investigating it compared to a control group that had smelled the same scent in a standard, non-playful cage.

    To understand what was happening in the brain at this two-month mark, the researchers looked at granule cells born on the mice’s first day of life. “Our results revealed an important role for neurons in the olfactory bulb that are generated at birth,” Mandairon said. “These neurons are highly plastic and, together with the brain’s reward system, contribute to the memory of an odor learned very early in life.”

    To test whether these neurons were strictly necessary for the memory, the scientists used optogenetics, a technique that allows researchers to turn specific brain cells on or off using light. When they used light to temporarily silence these early-born granule cells, the mice no longer showed a preference for the childhood scent.

    The researchers also examined broader brain activity in the young adult mice. They found that smelling the childhood odorant triggered highly synchronized activity between the brain’s reward centers and memory systems. This network included areas like the dorsal hippocampus, which is involved in detailed memories, and the medial prefrontal cortex, which handles complex decision-making.

    Next, the team investigated how this memory held up as the mice aged into later adulthood, at six months old. “We also found that, later in life, mice retained the memory of this odor only if they had been occasionally re-exposed to it during adulthood,” Mandairon told PsyPost. “Without such re-exposure, their preference for that particular odor disappeared.”

    However, if the researchers briefly re-exposed the mice to the scent every three weeks, the positive memory persisted at six months of age. Surprisingly, this long-lasting memory no longer relied on the neonatal granule cells in the olfactory bulb. The light-based silencing technique that worked at two months had no effect at six months.

    The researchers had expected a brain structure so directly involved in processing odors to continue playing a central role in olfactory memory. “Instead, over time, other brain circuits, particularly those associated with emotions, seem to take over,” Mandairon said.

    “What is particularly interesting is that the brain circuits supporting the memory appear to change over time,” she explained. “In adulthood, the contribution of the olfactory bulb and the reward system decreases, while regions of the limbic system, which is strongly involved in emotions, become more important. In other words, the memory can persist, but the brain mechanisms supporting it seem to evolve throughout life.”

    These network shifts are in line with a study covered by PsyPost in 2016, which found that early-life memories in young rats persist into adulthood as latent traces that can be reactivated by later reminder cues. The findings also align with another 2016 study covered by PsyPost, which found that worms form lifelong olfactory memories using specialized neural circuits. It is worth noting, however, that both of those previous studies examined the formation of aversive memories in response to threats, whereas the current study measured the development of positive odor associations in mice.

    One detail to keep in mind is that modeling human autobiographical memory in rodents comes with inherent limitations. “Although the anatomical and functional organization of the olfactory system shares many similarities between mice and humans, the study was conducted using a mouse model,” Mandairon cautioned. “Our study primarily allows us to identify general principles and brain mechanisms that can then be investigated further in humans.”

    Moving forward, the research team hopes to uncover the specific conditions that make some scent associations permanent while others fade. “We would like to determine whether there is a common ‘recipe’ that allows an odor encountered during childhood to become a memory that stays with us for a lifetime: what the odor was, the context in which it was encountered, who we were with, the emotions we experienced,” Mandairon said.

    The study, “Positive early-life olfactory memory is rooted in the olfactory bulb and triggers large-scale changes beyond the olfactory system,” was authored by Jules Dejou, Anna Athanassi, Théo Brunel, Marc Thevenet, Anne Didier, and Nathalie Mandairon.

    URL: psypost.org/neuroscientists-ma

    -------------------------------------------------

    Private, vetted email list for mental health professionals: 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 #OlfactoryMemory #EarlyLifeScent #Neuroscience #MemoryFormation #OlfactoryBulb #NeuralPlasticity #Hippocampus #LimbicSystem #MoodAndMemory #PLOSBiology

  11. DATE: August 25, 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: Neuroscientists map how early-life scent memories evolve and move through the brain

    URL: psypost.org/neuroscientists-ma

    The scent of a particular perfume or a childhood home can often bring back vivid, emotionally charged memories from a person’s earliest years. A recent study on mice suggests that these early-life scent memories are initially stored by specific neurons that develop just after birth, but as time passes and the scent is encountered again, the memory trace relocates to broader networks in the brain. The research, published in PLOS Biology, provides evidence for how the brain encodes, sustains, and eventually reorganizes our most cherished childhood memories.

    Scent-triggered memories are a well-documented psychological phenomenon, famously described by Marcel Proust as a flood of vivid nostalgic feelings brought on by the smell of a madeleine cake. In humans, autobiographical memories linked to scents tend to originate from the first decade of life. These memories also tend to carry a much stronger, more positive emotional tone than memories triggered by sights or sounds.

    Supporting this idea, a 2016 review indicated that scents tied to positive personal memories have a uniquely powerful impact on a person’s mood, often increasing positive emotions and reducing physiological signs of stress. Despite this well-known emotional potency, the exact ways the brain creates and stores these long-lasting scent memories have remained somewhat mysterious.

    When a person or animal smells something, the information first enters the olfactory bulb, a small structure at the front of the brain. Within this structure, specific neurons called granule cells help process the scent. In rodents, a massive wave of these granule cells is born on the very first day of life. Because these neonatal neurons are highly active during childhood and tend to survive for a long time, scientists suspected they might be ideal candidates for storing early-life scent memories.

    Memory researchers also know that the brain’s storage systems do not remain static. According to a framework discussed in a 2018 review, memories often shift between different brain areas as time passes. A memory might initially rely on specific regions, like the hippocampus, before being reorganized and transferred to broader networks in the brain’s outer layers.

    “I have been interested in odor perception and in the mechanisms of brain plasticity underlying olfactory learning since my PhD in Lyon, and later during my postdoctoral research at Cornell University,” said study author Nathalie Mandairon, a director of research at the French National Centre for Scientific Research (CNRS) based at the Lyon Neuroscience Research Center. “This study therefore follows naturally from my previous research.”

    “The question that particularly intrigued me was this: during childhood, we are exposed to a multitude of odors,” Mandairon continued. “Why do some of them remain embedded in our memory for decades, while others disappear? And what brain mechanisms allow these very early olfactory memories to persist or resurface later in life?”

    To find out, the research team began by surveying 647 adults about their earliest scent-based memories. “We found that this memory generally dated back to childhood, before the age of 10,” Mandairon explained. “They were most often associated with a pleasant odor, but also with a particularly positive, sometimes joyful, context.”

    “In most cases, the experience had also been repeated several times during childhood,” she added. “Based on these observations, we developed a mouse model to investigate the brain mechanisms involved in the formation and long-term maintenance of this early olfactory memory.”

    During the mouse equivalent of childhood, the researchers placed the animals in a large, enriched cage filled with toys, tunnels, and opportunities for social interaction. They paired this playful environment with a specific attractive odorant over five separate sessions. Microphones recorded the mice emitting a higher number and frequency of high-pitched squeaks, known as ultrasonic vocalizations, which indicates a positive emotional state.

    When the mice reached young adulthood, at two months of age, the researchers tested their reactions to the childhood odorant. The mice that had experienced the scent in the playful environment spent more time investigating it compared to a control group that had smelled the same scent in a standard, non-playful cage.

    To understand what was happening in the brain at this two-month mark, the researchers looked at granule cells born on the mice’s first day of life. “Our results revealed an important role for neurons in the olfactory bulb that are generated at birth,” Mandairon said. “These neurons are highly plastic and, together with the brain’s reward system, contribute to the memory of an odor learned very early in life.”

    To test whether these neurons were strictly necessary for the memory, the scientists used optogenetics, a technique that allows researchers to turn specific brain cells on or off using light. When they used light to temporarily silence these early-born granule cells, the mice no longer showed a preference for the childhood scent.

    The researchers also examined broader brain activity in the young adult mice. They found that smelling the childhood odorant triggered highly synchronized activity between the brain’s reward centers and memory systems. This network included areas like the dorsal hippocampus, which is involved in detailed memories, and the medial prefrontal cortex, which handles complex decision-making.

    Next, the team investigated how this memory held up as the mice aged into later adulthood, at six months old. “We also found that, later in life, mice retained the memory of this odor only if they had been occasionally re-exposed to it during adulthood,” Mandairon told PsyPost. “Without such re-exposure, their preference for that particular odor disappeared.”

    However, if the researchers briefly re-exposed the mice to the scent every three weeks, the positive memory persisted at six months of age. Surprisingly, this long-lasting memory no longer relied on the neonatal granule cells in the olfactory bulb. The light-based silencing technique that worked at two months had no effect at six months.

    The researchers had expected a brain structure so directly involved in processing odors to continue playing a central role in olfactory memory. “Instead, over time, other brain circuits, particularly those associated with emotions, seem to take over,” Mandairon said.

    “What is particularly interesting is that the brain circuits supporting the memory appear to change over time,” she explained. “In adulthood, the contribution of the olfactory bulb and the reward system decreases, while regions of the limbic system, which is strongly involved in emotions, become more important. In other words, the memory can persist, but the brain mechanisms supporting it seem to evolve throughout life.”

    These network shifts are in line with a study covered by PsyPost in 2016, which found that early-life memories in young rats persist into adulthood as latent traces that can be reactivated by later reminder cues. The findings also align with another 2016 study covered by PsyPost, which found that worms form lifelong olfactory memories using specialized neural circuits. It is worth noting, however, that both of those previous studies examined the formation of aversive memories in response to threats, whereas the current study measured the development of positive odor associations in mice.

    One detail to keep in mind is that modeling human autobiographical memory in rodents comes with inherent limitations. “Although the anatomical and functional organization of the olfactory system shares many similarities between mice and humans, the study was conducted using a mouse model,” Mandairon cautioned. “Our study primarily allows us to identify general principles and brain mechanisms that can then be investigated further in humans.”

    Moving forward, the research team hopes to uncover the specific conditions that make some scent associations permanent while others fade. “We would like to determine whether there is a common ‘recipe’ that allows an odor encountered during childhood to become a memory that stays with us for a lifetime: what the odor was, the context in which it was encountered, who we were with, the emotions we experienced,” Mandairon said.

    The study, “Positive early-life olfactory memory is rooted in the olfactory bulb and triggers large-scale changes beyond the olfactory system,” was authored by Jules Dejou, Anna Athanassi, Théo Brunel, Marc Thevenet, Anne Didier, and Nathalie Mandairon.

    URL: psypost.org/neuroscientists-ma

    -------------------------------------------------

    Private, vetted email list for mental health professionals: 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 #OlfactoryMemory #EarlyLifeScent #Neuroscience #MemoryFormation #OlfactoryBulb #NeuralPlasticity #Hippocampus #LimbicSystem #MoodAndMemory #PLOSBiology

  12. DATE: August 25, 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: Neuroscientists map how early-life scent memories evolve and move through the brain

    URL: psypost.org/neuroscientists-ma

    The scent of a particular perfume or a childhood home can often bring back vivid, emotionally charged memories from a person’s earliest years. A recent study on mice suggests that these early-life scent memories are initially stored by specific neurons that develop just after birth, but as time passes and the scent is encountered again, the memory trace relocates to broader networks in the brain. The research, published in PLOS Biology, provides evidence for how the brain encodes, sustains, and eventually reorganizes our most cherished childhood memories.

    Scent-triggered memories are a well-documented psychological phenomenon, famously described by Marcel Proust as a flood of vivid nostalgic feelings brought on by the smell of a madeleine cake. In humans, autobiographical memories linked to scents tend to originate from the first decade of life. These memories also tend to carry a much stronger, more positive emotional tone than memories triggered by sights or sounds.

    Supporting this idea, a 2016 review indicated that scents tied to positive personal memories have a uniquely powerful impact on a person’s mood, often increasing positive emotions and reducing physiological signs of stress. Despite this well-known emotional potency, the exact ways the brain creates and stores these long-lasting scent memories have remained somewhat mysterious.

    When a person or animal smells something, the information first enters the olfactory bulb, a small structure at the front of the brain. Within this structure, specific neurons called granule cells help process the scent. In rodents, a massive wave of these granule cells is born on the very first day of life. Because these neonatal neurons are highly active during childhood and tend to survive for a long time, scientists suspected they might be ideal candidates for storing early-life scent memories.

    Memory researchers also know that the brain’s storage systems do not remain static. According to a framework discussed in a 2018 review, memories often shift between different brain areas as time passes. A memory might initially rely on specific regions, like the hippocampus, before being reorganized and transferred to broader networks in the brain’s outer layers.

    “I have been interested in odor perception and in the mechanisms of brain plasticity underlying olfactory learning since my PhD in Lyon, and later during my postdoctoral research at Cornell University,” said study author Nathalie Mandairon, a director of research at the French National Centre for Scientific Research (CNRS) based at the Lyon Neuroscience Research Center. “This study therefore follows naturally from my previous research.”

    “The question that particularly intrigued me was this: during childhood, we are exposed to a multitude of odors,” Mandairon continued. “Why do some of them remain embedded in our memory for decades, while others disappear? And what brain mechanisms allow these very early olfactory memories to persist or resurface later in life?”

    To find out, the research team began by surveying 647 adults about their earliest scent-based memories. “We found that this memory generally dated back to childhood, before the age of 10,” Mandairon explained. “They were most often associated with a pleasant odor, but also with a particularly positive, sometimes joyful, context.”

    “In most cases, the experience had also been repeated several times during childhood,” she added. “Based on these observations, we developed a mouse model to investigate the brain mechanisms involved in the formation and long-term maintenance of this early olfactory memory.”

    During the mouse equivalent of childhood, the researchers placed the animals in a large, enriched cage filled with toys, tunnels, and opportunities for social interaction. They paired this playful environment with a specific attractive odorant over five separate sessions. Microphones recorded the mice emitting a higher number and frequency of high-pitched squeaks, known as ultrasonic vocalizations, which indicates a positive emotional state.

    When the mice reached young adulthood, at two months of age, the researchers tested their reactions to the childhood odorant. The mice that had experienced the scent in the playful environment spent more time investigating it compared to a control group that had smelled the same scent in a standard, non-playful cage.

    To understand what was happening in the brain at this two-month mark, the researchers looked at granule cells born on the mice’s first day of life. “Our results revealed an important role for neurons in the olfactory bulb that are generated at birth,” Mandairon said. “These neurons are highly plastic and, together with the brain’s reward system, contribute to the memory of an odor learned very early in life.”

    To test whether these neurons were strictly necessary for the memory, the scientists used optogenetics, a technique that allows researchers to turn specific brain cells on or off using light. When they used light to temporarily silence these early-born granule cells, the mice no longer showed a preference for the childhood scent.

    The researchers also examined broader brain activity in the young adult mice. They found that smelling the childhood odorant triggered highly synchronized activity between the brain’s reward centers and memory systems. This network included areas like the dorsal hippocampus, which is involved in detailed memories, and the medial prefrontal cortex, which handles complex decision-making.

    Next, the team investigated how this memory held up as the mice aged into later adulthood, at six months old. “We also found that, later in life, mice retained the memory of this odor only if they had been occasionally re-exposed to it during adulthood,” Mandairon told PsyPost. “Without such re-exposure, their preference for that particular odor disappeared.”

    However, if the researchers briefly re-exposed the mice to the scent every three weeks, the positive memory persisted at six months of age. Surprisingly, this long-lasting memory no longer relied on the neonatal granule cells in the olfactory bulb. The light-based silencing technique that worked at two months had no effect at six months.

    The researchers had expected a brain structure so directly involved in processing odors to continue playing a central role in olfactory memory. “Instead, over time, other brain circuits, particularly those associated with emotions, seem to take over,” Mandairon said.

    “What is particularly interesting is that the brain circuits supporting the memory appear to change over time,” she explained. “In adulthood, the contribution of the olfactory bulb and the reward system decreases, while regions of the limbic system, which is strongly involved in emotions, become more important. In other words, the memory can persist, but the brain mechanisms supporting it seem to evolve throughout life.”

    These network shifts are in line with a study covered by PsyPost in 2016, which found that early-life memories in young rats persist into adulthood as latent traces that can be reactivated by later reminder cues. The findings also align with another 2016 study covered by PsyPost, which found that worms form lifelong olfactory memories using specialized neural circuits. It is worth noting, however, that both of those previous studies examined the formation of aversive memories in response to threats, whereas the current study measured the development of positive odor associations in mice.

    One detail to keep in mind is that modeling human autobiographical memory in rodents comes with inherent limitations. “Although the anatomical and functional organization of the olfactory system shares many similarities between mice and humans, the study was conducted using a mouse model,” Mandairon cautioned. “Our study primarily allows us to identify general principles and brain mechanisms that can then be investigated further in humans.”

    Moving forward, the research team hopes to uncover the specific conditions that make some scent associations permanent while others fade. “We would like to determine whether there is a common ‘recipe’ that allows an odor encountered during childhood to become a memory that stays with us for a lifetime: what the odor was, the context in which it was encountered, who we were with, the emotions we experienced,” Mandairon said.

    The study, “Positive early-life olfactory memory is rooted in the olfactory bulb and triggers large-scale changes beyond the olfactory system,” was authored by Jules Dejou, Anna Athanassi, Théo Brunel, Marc Thevenet, Anne Didier, and Nathalie Mandairon.

    URL: psypost.org/neuroscientists-ma

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    #psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #OlfactoryMemory #EarlyLifeScent #Neuroscience #MemoryFormation #OlfactoryBulb #NeuralPlasticity #Hippocampus #LimbicSystem #MoodAndMemory #PLOSBiology

  13. DATE: August 25, 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: Neuroscientists map how early-life scent memories evolve and move through the brain

    URL: psypost.org/neuroscientists-ma

    The scent of a particular perfume or a childhood home can often bring back vivid, emotionally charged memories from a person’s earliest years. A recent study on mice suggests that these early-life scent memories are initially stored by specific neurons that develop just after birth, but as time passes and the scent is encountered again, the memory trace relocates to broader networks in the brain. The research, published in PLOS Biology, provides evidence for how the brain encodes, sustains, and eventually reorganizes our most cherished childhood memories.

    Scent-triggered memories are a well-documented psychological phenomenon, famously described by Marcel Proust as a flood of vivid nostalgic feelings brought on by the smell of a madeleine cake. In humans, autobiographical memories linked to scents tend to originate from the first decade of life. These memories also tend to carry a much stronger, more positive emotional tone than memories triggered by sights or sounds.

    Supporting this idea, a 2016 review indicated that scents tied to positive personal memories have a uniquely powerful impact on a person’s mood, often increasing positive emotions and reducing physiological signs of stress. Despite this well-known emotional potency, the exact ways the brain creates and stores these long-lasting scent memories have remained somewhat mysterious.

    When a person or animal smells something, the information first enters the olfactory bulb, a small structure at the front of the brain. Within this structure, specific neurons called granule cells help process the scent. In rodents, a massive wave of these granule cells is born on the very first day of life. Because these neonatal neurons are highly active during childhood and tend to survive for a long time, scientists suspected they might be ideal candidates for storing early-life scent memories.

    Memory researchers also know that the brain’s storage systems do not remain static. According to a framework discussed in a 2018 review, memories often shift between different brain areas as time passes. A memory might initially rely on specific regions, like the hippocampus, before being reorganized and transferred to broader networks in the brain’s outer layers.

    “I have been interested in odor perception and in the mechanisms of brain plasticity underlying olfactory learning since my PhD in Lyon, and later during my postdoctoral research at Cornell University,” said study author Nathalie Mandairon, a director of research at the French National Centre for Scientific Research (CNRS) based at the Lyon Neuroscience Research Center. “This study therefore follows naturally from my previous research.”

    “The question that particularly intrigued me was this: during childhood, we are exposed to a multitude of odors,” Mandairon continued. “Why do some of them remain embedded in our memory for decades, while others disappear? And what brain mechanisms allow these very early olfactory memories to persist or resurface later in life?”

    To find out, the research team began by surveying 647 adults about their earliest scent-based memories. “We found that this memory generally dated back to childhood, before the age of 10,” Mandairon explained. “They were most often associated with a pleasant odor, but also with a particularly positive, sometimes joyful, context.”

    “In most cases, the experience had also been repeated several times during childhood,” she added. “Based on these observations, we developed a mouse model to investigate the brain mechanisms involved in the formation and long-term maintenance of this early olfactory memory.”

    During the mouse equivalent of childhood, the researchers placed the animals in a large, enriched cage filled with toys, tunnels, and opportunities for social interaction. They paired this playful environment with a specific attractive odorant over five separate sessions. Microphones recorded the mice emitting a higher number and frequency of high-pitched squeaks, known as ultrasonic vocalizations, which indicates a positive emotional state.

    When the mice reached young adulthood, at two months of age, the researchers tested their reactions to the childhood odorant. The mice that had experienced the scent in the playful environment spent more time investigating it compared to a control group that had smelled the same scent in a standard, non-playful cage.

    To understand what was happening in the brain at this two-month mark, the researchers looked at granule cells born on the mice’s first day of life. “Our results revealed an important role for neurons in the olfactory bulb that are generated at birth,” Mandairon said. “These neurons are highly plastic and, together with the brain’s reward system, contribute to the memory of an odor learned very early in life.”

    To test whether these neurons were strictly necessary for the memory, the scientists used optogenetics, a technique that allows researchers to turn specific brain cells on or off using light. When they used light to temporarily silence these early-born granule cells, the mice no longer showed a preference for the childhood scent.

    The researchers also examined broader brain activity in the young adult mice. They found that smelling the childhood odorant triggered highly synchronized activity between the brain’s reward centers and memory systems. This network included areas like the dorsal hippocampus, which is involved in detailed memories, and the medial prefrontal cortex, which handles complex decision-making.

    Next, the team investigated how this memory held up as the mice aged into later adulthood, at six months old. “We also found that, later in life, mice retained the memory of this odor only if they had been occasionally re-exposed to it during adulthood,” Mandairon told PsyPost. “Without such re-exposure, their preference for that particular odor disappeared.”

    However, if the researchers briefly re-exposed the mice to the scent every three weeks, the positive memory persisted at six months of age. Surprisingly, this long-lasting memory no longer relied on the neonatal granule cells in the olfactory bulb. The light-based silencing technique that worked at two months had no effect at six months.

    The researchers had expected a brain structure so directly involved in processing odors to continue playing a central role in olfactory memory. “Instead, over time, other brain circuits, particularly those associated with emotions, seem to take over,” Mandairon said.

    “What is particularly interesting is that the brain circuits supporting the memory appear to change over time,” she explained. “In adulthood, the contribution of the olfactory bulb and the reward system decreases, while regions of the limbic system, which is strongly involved in emotions, become more important. In other words, the memory can persist, but the brain mechanisms supporting it seem to evolve throughout life.”

    These network shifts are in line with a study covered by PsyPost in 2016, which found that early-life memories in young rats persist into adulthood as latent traces that can be reactivated by later reminder cues. The findings also align with another 2016 study covered by PsyPost, which found that worms form lifelong olfactory memories using specialized neural circuits. It is worth noting, however, that both of those previous studies examined the formation of aversive memories in response to threats, whereas the current study measured the development of positive odor associations in mice.

    One detail to keep in mind is that modeling human autobiographical memory in rodents comes with inherent limitations. “Although the anatomical and functional organization of the olfactory system shares many similarities between mice and humans, the study was conducted using a mouse model,” Mandairon cautioned. “Our study primarily allows us to identify general principles and brain mechanisms that can then be investigated further in humans.”

    Moving forward, the research team hopes to uncover the specific conditions that make some scent associations permanent while others fade. “We would like to determine whether there is a common ‘recipe’ that allows an odor encountered during childhood to become a memory that stays with us for a lifetime: what the odor was, the context in which it was encountered, who we were with, the emotions we experienced,” Mandairon said.

    The study, “Positive early-life olfactory memory is rooted in the olfactory bulb and triggers large-scale changes beyond the olfactory system,” was authored by Jules Dejou, Anna Athanassi, Théo Brunel, Marc Thevenet, Anne Didier, and Nathalie Mandairon.

    URL: psypost.org/neuroscientists-ma

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    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 #OlfactoryMemory #EarlyLifeScent #Neuroscience #MemoryFormation #OlfactoryBulb #NeuralPlasticity #Hippocampus #LimbicSystem #MoodAndMemory #PLOSBiology

  14. New preprint dropped: __Systemic diazepam alters local hippocampal CA1 circuits and differentially affects entorhinal and CA3 inputs__

    Peterson et al. (2026) #bioRxiv

    biorxiv.org/content/10.64898/2

    Really cool and amazing results that systemic diazepam obliterates hippocampal #sharpWaveRipples in vivo, particularly during the post-task rest, and disrupts representations during running.

    Implies important issues that diazepam's side effects on consolidation really ought to be looked at. (All the diazepam memory tests we could find in the literature are short-term tests, no one seems to have looked at long-term consolidation, but would love citations if people have them.)

    PS. To be honest, though, my favorite figure is the proof-of-efficacy in Figure 2 where decreased spiking cross-correlation directly reveals diazepam's effects on inhibition. It's so clean!

    #science #neuroscience #hippocampus

  15. New preprint dropped: __Systemic diazepam alters local hippocampal CA1 circuits and differentially affects entorhinal and CA3 inputs__

    Peterson et al. (2026) #bioRxiv

    biorxiv.org/content/10.64898/2

    Really cool and amazing results that systemic diazepam obliterates hippocampal #sharpWaveRipples in vivo, particularly during the post-task rest, and disrupts representations during running.

    Implies important issues that diazepam's side effects on consolidation really ought to be looked at. (All the diazepam memory tests we could find in the literature are short-term tests, no one seems to have looked at long-term consolidation, but would love citations if people have them.)

    PS. To be honest, though, my favorite figure is the proof-of-efficacy in Figure 2 where decreased spiking cross-correlation directly reveals diazepam's effects on inhibition. It's so clean!

    #science #neuroscience #hippocampus

  16. New preprint dropped: __Systemic diazepam alters local hippocampal CA1 circuits and differentially affects entorhinal and CA3 inputs__

    Peterson et al. (2026) #bioRxiv

    biorxiv.org/content/10.64898/2

    Really cool and amazing results that systemic diazepam obliterates hippocampal #sharpWaveRipples in vivo, particularly during the post-task rest, and disrupts representations during running.

    Implies important issues that diazepam's side effects on consolidation really ought to be looked at. (All the diazepam memory tests we could find in the literature are short-term tests, no one seems to have looked at long-term consolidation, but would love citations if people have them.)

    PS. To be honest, though, my favorite figure is the proof-of-efficacy in Figure 2 where decreased spiking cross-correlation directly reveals diazepam's effects on inhibition. It's so clean!

    #science #neuroscience #hippocampus

  17. New preprint dropped: __Systemic diazepam alters local hippocampal CA1 circuits and differentially affects entorhinal and CA3 inputs__

    Peterson et al. (2026) #bioRxiv

    biorxiv.org/content/10.64898/2

    Really cool and amazing results that systemic diazepam obliterates hippocampal #sharpWaveRipples in vivo, particularly during the post-task rest, and disrupts representations during running.

    Implies important issues that diazepam's side effects on consolidation really ought to be looked at. (All the diazepam memory tests we could find in the literature are short-term tests, no one seems to have looked at long-term consolidation, but would love citations if people have them.)

    PS. To be honest, though, my favorite figure is the proof-of-efficacy in Figure 2 where decreased spiking cross-correlation directly reveals diazepam's effects on inhibition. It's so clean!

    #science #neuroscience #hippocampus

  18. New preprint dropped: __Systemic diazepam alters local hippocampal CA1 circuits and differentially affects entorhinal and CA3 inputs__

    Peterson et al. (2026) #bioRxiv

    biorxiv.org/content/10.64898/2

    Really cool and amazing results that systemic diazepam obliterates hippocampal #sharpWaveRipples in vivo, particularly during the post-task rest, and disrupts representations during running.

    Implies important issues that diazepam's side effects on consolidation really ought to be looked at. (All the diazepam memory tests we could find in the literature are short-term tests, no one seems to have looked at long-term consolidation, but would love citations if people have them.)

    PS. To be honest, though, my favorite figure is the proof-of-efficacy in Figure 2 where decreased spiking cross-correlation directly reveals diazepam's effects on inhibition. It's so clean!

    #science #neuroscience #hippocampus

  19. A study of gene expression in cells of the hippocampus in patients with major depressive disorder found that, in comparison to controls, depression as associated with a reduction in neurogenesis.

    Summary: medicalxpress.com/news/2026-08

    Original paper: nature.com/articles/s41591-026

    #Science #MentalHealth #Depression #Hippocampus #Neurogenesis

  20. A study of gene expression in cells of the hippocampus in patients with major depressive disorder found that, in comparison to controls, depression as associated with a reduction in neurogenesis.

    Summary: medicalxpress.com/news/2026-08

    Original paper: nature.com/articles/s41591-026

    #Science #MentalHealth #Depression #Hippocampus #Neurogenesis

  21. A study of gene expression in cells of the hippocampus in patients with major depressive disorder found that, in comparison to controls, depression as associated with a reduction in neurogenesis.

    Summary: medicalxpress.com/news/2026-08

    Original paper: nature.com/articles/s41591-026

    #Science #MentalHealth #Depression #Hippocampus #Neurogenesis

  22. A study of gene expression in cells of the hippocampus in patients with major depressive disorder found that, in comparison to controls, depression as associated with a reduction in neurogenesis.

    Summary: medicalxpress.com/news/2026-08

    Original paper: nature.com/articles/s41591-026

    #Science #MentalHealth #Depression #Hippocampus #Neurogenesis

  23. A study of gene expression in cells of the hippocampus in patients with major depressive disorder found that, in comparison to controls, depression as associated with a reduction in neurogenesis.

    Summary: medicalxpress.com/news/2026-08

    Original paper: nature.com/articles/s41591-026

    #Science #MentalHealth #Depression #Hippocampus #Neurogenesis

  24. @elduvelle_neuro As a physicist, I’d say…I mean, the direction is at least correct, isn’t it? It’s pointing toward the 🐁‘s front end. Everything beyond…that’s probably a matter for the #hippocampus crowd 😅

  25. @elduvelle_neuro As a physicist, I’d say…I mean, the direction is at least correct, isn’t it? It’s pointing toward the 🐁‘s front end. Everything beyond…that’s probably a matter for the #hippocampus crowd 😅

  26. @elduvelle_neuro As a physicist, I’d say…I mean, the direction is at least correct, isn’t it? It’s pointing toward the 🐁‘s front end. Everything beyond…that’s probably a matter for the #hippocampus crowd 😅

  27. @elduvelle_neuro As a physicist, I’d say…I mean, the direction is at least correct, isn’t it? It’s pointing toward the 🐁‘s front end. Everything beyond…that’s probably a matter for the #hippocampus crowd 😅

  28. @elduvelle_neuro As a physicist, I’d say…I mean, the direction is at least correct, isn’t it? It’s pointing toward the 🐁‘s front end. Everything beyond…that’s probably a matter for the #hippocampus crowd 😅

  29. DATE: August 15, 2026 at 04:00PM
    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: Adolescent binge drinking permanently alters adult brain sensitivity to alcohol

    URL: psypost.org/adolescent-binge-d

    Heavy drinking during adolescence may leave the adult brain unusually sensitive to alcohol, according to a study published in Molecular Psychiatry. Experiments in male mice found that binge-like drinking during adolescence permanently changed how alcohol affected hippocampal nerve cells, although the altered response was reduced by the medication baclofen.

    Adolescence is a period of rapid brain development. Systems involved in seeking rewards become highly active during the teenage years, while brain regions responsible for planning and self-control continue maturing. This imbalance may make adolescents more likely to take risks, including consuming large amounts of alcohol in a short period.

    Previous animal studies have linked heavy adolescent drinking with lasting changes in memory, anxiety, impulsivity, and responses to alcohol. However, scientists have known less about the specific cellular processes that could make the developing brain especially vulnerable.

    The new study focused on GIRK channels, which are structures in nerve cells that allow potassium to move across the cell membrane. Their activity generally makes nerve cells less likely to fire. Alcohol can activate these channels, helping produce some of alcohol’s effects on the brain. The researchers also examined activin A, a signaling protein involved in brain development, learning, and emotional behavior.

    In the study conducted by researchers at Friedrich-Alexander University of Erlangen–Nuremberg, Germany, the team worked with male mice. The animals were either adolescents, approximately 30 to 45 days old, or adults aged three to five months. Adolescent mice were given access to 20% alcohol during their active period for about two weeks. They were then kept alcohol-free until adulthood.

    Electrical activity was recorded from nerve cells in the hippocampus, a brain region important for memory and involved in alcohol-related effects. In mice that had never consumed alcohol, activin A had opposite effects depending on age. It increased the cells’ sensitivity to alcohol during adolescence but reduced alcohol sensitivity in adulthood.

    This developmental change normally acted like a switch. However, mice that had consumed alcohol heavily during adolescence did not show the usual adult response. Even after a lengthy alcohol-free period, their adult hippocampal cells remained highly sensitive to alcohol.

    The altered cells showed stronger GIRK channel activity and became less likely to fire when exposed to alcohol. In some experiments, alcohol suppressed the firing of most tested nerve cells from mice with adolescent drinking experience.

    The team also tested baclofen, a drug that activates GIRK channels and is sometimes prescribed off-label (meaning it is used for a condition it was not officially approved to treat) for alcohol use disorders. In the mouse brain slices, baclofen reduced the unusually large alcohol-induced GIRK response seen after adolescent drinking. The researchers noted: “This finding introduces not only a putative [proposed] new mechanism of therapeutic action, but, with the hippocampus, also a new site of action, with direct implications for [alcohol use disorder]-associated cognitive deficits and affective [mood] disorders.”

    The study has several important limitations. For instance, the experiments focused mainly on the hippocampus, while alcohol affects many brain areas. Additionally, the study utilized mice exposed to alcohol for only two weeks, and thus its drinking model may not reflect the variety, duration, or social context of adolescent alcohol use in humans.

    The study, “Heavy adolescent drinking makes the adult brain more vulnerable to ethanol by permanently altering the age-dependent interplay between alcohol, GIRK channels and activin,” was authored by Sophia Stürzenberger, Nicolas Bülow, Liubov S. Kalinichenko, Rebecca Licha, Volker Eulenburg, Marc Dahlmanns, Christian P. Müller, Fang Zheng, and Christian Alzheimer.

    URL: psypost.org/adolescent-binge-d

    -------------------------------------------------

    Private, vetted email list for mental health professionals: 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 #AdolescentDrinking #AlcoholResearch #BrainDevelopment #GIRKChannels #ActivinA #Hippocampus #AlcoholSensitivity #Baclofen #MolecularPsychiatry #ADHDtoAlcoholImpact

  30. DATE: August 15, 2026 at 04:00PM
    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: Adolescent binge drinking permanently alters adult brain sensitivity to alcohol

    URL: psypost.org/adolescent-binge-d

    Heavy drinking during adolescence may leave the adult brain unusually sensitive to alcohol, according to a study published in Molecular Psychiatry. Experiments in male mice found that binge-like drinking during adolescence permanently changed how alcohol affected hippocampal nerve cells, although the altered response was reduced by the medication baclofen.

    Adolescence is a period of rapid brain development. Systems involved in seeking rewards become highly active during the teenage years, while brain regions responsible for planning and self-control continue maturing. This imbalance may make adolescents more likely to take risks, including consuming large amounts of alcohol in a short period.

    Previous animal studies have linked heavy adolescent drinking with lasting changes in memory, anxiety, impulsivity, and responses to alcohol. However, scientists have known less about the specific cellular processes that could make the developing brain especially vulnerable.

    The new study focused on GIRK channels, which are structures in nerve cells that allow potassium to move across the cell membrane. Their activity generally makes nerve cells less likely to fire. Alcohol can activate these channels, helping produce some of alcohol’s effects on the brain. The researchers also examined activin A, a signaling protein involved in brain development, learning, and emotional behavior.

    In the study conducted by researchers at Friedrich-Alexander University of Erlangen–Nuremberg, Germany, the team worked with male mice. The animals were either adolescents, approximately 30 to 45 days old, or adults aged three to five months. Adolescent mice were given access to 20% alcohol during their active period for about two weeks. They were then kept alcohol-free until adulthood.

    Electrical activity was recorded from nerve cells in the hippocampus, a brain region important for memory and involved in alcohol-related effects. In mice that had never consumed alcohol, activin A had opposite effects depending on age. It increased the cells’ sensitivity to alcohol during adolescence but reduced alcohol sensitivity in adulthood.

    This developmental change normally acted like a switch. However, mice that had consumed alcohol heavily during adolescence did not show the usual adult response. Even after a lengthy alcohol-free period, their adult hippocampal cells remained highly sensitive to alcohol.

    The altered cells showed stronger GIRK channel activity and became less likely to fire when exposed to alcohol. In some experiments, alcohol suppressed the firing of most tested nerve cells from mice with adolescent drinking experience.

    The team also tested baclofen, a drug that activates GIRK channels and is sometimes prescribed off-label (meaning it is used for a condition it was not officially approved to treat) for alcohol use disorders. In the mouse brain slices, baclofen reduced the unusually large alcohol-induced GIRK response seen after adolescent drinking. The researchers noted: “This finding introduces not only a putative [proposed] new mechanism of therapeutic action, but, with the hippocampus, also a new site of action, with direct implications for [alcohol use disorder]-associated cognitive deficits and affective [mood] disorders.”

    The study has several important limitations. For instance, the experiments focused mainly on the hippocampus, while alcohol affects many brain areas. Additionally, the study utilized mice exposed to alcohol for only two weeks, and thus its drinking model may not reflect the variety, duration, or social context of adolescent alcohol use in humans.

    The study, “Heavy adolescent drinking makes the adult brain more vulnerable to ethanol by permanently altering the age-dependent interplay between alcohol, GIRK channels and activin,” was authored by Sophia Stürzenberger, Nicolas Bülow, Liubov S. Kalinichenko, Rebecca Licha, Volker Eulenburg, Marc Dahlmanns, Christian P. Müller, Fang Zheng, and Christian Alzheimer.

    URL: psypost.org/adolescent-binge-d

    -------------------------------------------------

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    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 #AdolescentDrinking #AlcoholResearch #BrainDevelopment #GIRKChannels #ActivinA #Hippocampus #AlcoholSensitivity #Baclofen #MolecularPsychiatry #ADHDtoAlcoholImpact

  31. DATE: August 15, 2026 at 04:00PM
    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: Adolescent binge drinking permanently alters adult brain sensitivity to alcohol

    URL: psypost.org/adolescent-binge-d

    Heavy drinking during adolescence may leave the adult brain unusually sensitive to alcohol, according to a study published in Molecular Psychiatry. Experiments in male mice found that binge-like drinking during adolescence permanently changed how alcohol affected hippocampal nerve cells, although the altered response was reduced by the medication baclofen.

    Adolescence is a period of rapid brain development. Systems involved in seeking rewards become highly active during the teenage years, while brain regions responsible for planning and self-control continue maturing. This imbalance may make adolescents more likely to take risks, including consuming large amounts of alcohol in a short period.

    Previous animal studies have linked heavy adolescent drinking with lasting changes in memory, anxiety, impulsivity, and responses to alcohol. However, scientists have known less about the specific cellular processes that could make the developing brain especially vulnerable.

    The new study focused on GIRK channels, which are structures in nerve cells that allow potassium to move across the cell membrane. Their activity generally makes nerve cells less likely to fire. Alcohol can activate these channels, helping produce some of alcohol’s effects on the brain. The researchers also examined activin A, a signaling protein involved in brain development, learning, and emotional behavior.

    In the study conducted by researchers at Friedrich-Alexander University of Erlangen–Nuremberg, Germany, the team worked with male mice. The animals were either adolescents, approximately 30 to 45 days old, or adults aged three to five months. Adolescent mice were given access to 20% alcohol during their active period for about two weeks. They were then kept alcohol-free until adulthood.

    Electrical activity was recorded from nerve cells in the hippocampus, a brain region important for memory and involved in alcohol-related effects. In mice that had never consumed alcohol, activin A had opposite effects depending on age. It increased the cells’ sensitivity to alcohol during adolescence but reduced alcohol sensitivity in adulthood.

    This developmental change normally acted like a switch. However, mice that had consumed alcohol heavily during adolescence did not show the usual adult response. Even after a lengthy alcohol-free period, their adult hippocampal cells remained highly sensitive to alcohol.

    The altered cells showed stronger GIRK channel activity and became less likely to fire when exposed to alcohol. In some experiments, alcohol suppressed the firing of most tested nerve cells from mice with adolescent drinking experience.

    The team also tested baclofen, a drug that activates GIRK channels and is sometimes prescribed off-label (meaning it is used for a condition it was not officially approved to treat) for alcohol use disorders. In the mouse brain slices, baclofen reduced the unusually large alcohol-induced GIRK response seen after adolescent drinking. The researchers noted: “This finding introduces not only a putative [proposed] new mechanism of therapeutic action, but, with the hippocampus, also a new site of action, with direct implications for [alcohol use disorder]-associated cognitive deficits and affective [mood] disorders.”

    The study has several important limitations. For instance, the experiments focused mainly on the hippocampus, while alcohol affects many brain areas. Additionally, the study utilized mice exposed to alcohol for only two weeks, and thus its drinking model may not reflect the variety, duration, or social context of adolescent alcohol use in humans.

    The study, “Heavy adolescent drinking makes the adult brain more vulnerable to ethanol by permanently altering the age-dependent interplay between alcohol, GIRK channels and activin,” was authored by Sophia Stürzenberger, Nicolas Bülow, Liubov S. Kalinichenko, Rebecca Licha, Volker Eulenburg, Marc Dahlmanns, Christian P. Müller, Fang Zheng, and Christian Alzheimer.

    URL: psypost.org/adolescent-binge-d

    -------------------------------------------------

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    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 #AdolescentDrinking #AlcoholResearch #BrainDevelopment #GIRKChannels #ActivinA #Hippocampus #AlcoholSensitivity #Baclofen #MolecularPsychiatry #ADHDtoAlcoholImpact

  32. Taxi Drivers Rarely Die Of Alzheimer’s – How Complex Mental Maps And Spatial Reasoning Protect Your Brain [why knowing your way around might help you stay sharp]
    --
    theconversation.com/taxi-drive <-- shared technical article
    --
    doi.org/10.1136/bmj-2024-082194 <-- shared paper
    --
    doi.org/10.1073/pnas.070039597 <-- shared paper
    --
    doi.org/10.1038/s41582-018-003 <-- shared paper
    --
    tfl.gov.uk/info-for/taxis-and- <-- details of @Transport for London’s ‘The Knowledge’ details
    --
    youtu.be/u7gp8KBP7ak?si=X1xXcy <-- shared video, ‘The People Who Have To Remember 25,000 Streets | The [London] Knowledge - The World's Toughest Taxi Test’
    --
    H/T @ Jennifer Psillas, GISP | GIS Project Manager at City of Tucson Parks and Recreation
    “Taxi and ambulance drivers are less likely than workers in almost any other job to die of Alzheimer’s disease. That was the surprising result of a 2024 study examining the death certificates of nearly 9 million people in the U.S…
    Of the 9 million death certificates from January 2020 to December 2022 that researchers examined, taxi and ambulance drivers had the lowest risk of dying from Alzheimer’s disease out of 443 occupations. After adjusting for age, sex, race, ethnicity and education, roughly 1 in 100 taxi and ambulance drivers died of Alzheimer’s, compared with 1 in 60 people overall.
    This pattern did not extend to other driving jobs. The researchers concluded that the key to reducing the risk of Alzheimer’s was not driving itself but continuous real-time navigation: the constant work of locating yourself in space, tracking a destination and updating a mental map as conditions change. Drivers whose jobs relied on fixed or predetermined routes, like bus drivers and aircraft pilots, didn’t seem to experience a similar advantage.
    Researchers believe the association between navigation-heavy work and lower Alzheimer’s risk centers on the hippocampus, a part of the brain that governs memory and spatial navigation. It’s one of the first brain regions that Alzheimer’s damages: Problems with spatial navigation and orientation are among the earliest signs of the disease, sometimes surfacing before obvious memory loss.
    In one landmark 2000 study [link above], neuroscientists compared the brains of licensed London taxi drivers with those of people who did not drive cabs. Their findings provided the first evidence via structural imaging that regions of the adult brain can measurably change under sustained navigational demand. To earn a license, London cabbies must memorize more than 25,000 streets within a 6-mile radius of Charing Cross, a challenge known as “The Knowledge” that takes three to four years…”
    #spatialnavigation #orientation #mental #acuity #taxi #ambulance #paramedic #TheKnowledge #London #UK #Alzheimer #mapping #mentalmaps #spatialmapping #navigation #spatialreasoning #brain #hippocampus #brainhealth #death #mortality #disease #publichealth #scans #occupation #job

  33. Taxi Drivers Rarely Die Of Alzheimer’s – How Complex Mental Maps And Spatial Reasoning Protect Your Brain [why knowing your way around might help you stay sharp]
    --
    theconversation.com/taxi-drive <-- shared technical article
    --
    doi.org/10.1136/bmj-2024-082194 <-- shared paper
    --
    doi.org/10.1073/pnas.070039597 <-- shared paper
    --
    doi.org/10.1038/s41582-018-003 <-- shared paper
    --
    tfl.gov.uk/info-for/taxis-and- <-- details of @Transport for London’s ‘The Knowledge’ details
    --
    youtu.be/u7gp8KBP7ak?si=X1xXcy <-- shared video, ‘The People Who Have To Remember 25,000 Streets | The [London] Knowledge - The World's Toughest Taxi Test’
    --
    H/T @ Jennifer Psillas, GISP | GIS Project Manager at City of Tucson Parks and Recreation
    “Taxi and ambulance drivers are less likely than workers in almost any other job to die of Alzheimer’s disease. That was the surprising result of a 2024 study examining the death certificates of nearly 9 million people in the U.S…
    Of the 9 million death certificates from January 2020 to December 2022 that researchers examined, taxi and ambulance drivers had the lowest risk of dying from Alzheimer’s disease out of 443 occupations. After adjusting for age, sex, race, ethnicity and education, roughly 1 in 100 taxi and ambulance drivers died of Alzheimer’s, compared with 1 in 60 people overall.
    This pattern did not extend to other driving jobs. The researchers concluded that the key to reducing the risk of Alzheimer’s was not driving itself but continuous real-time navigation: the constant work of locating yourself in space, tracking a destination and updating a mental map as conditions change. Drivers whose jobs relied on fixed or predetermined routes, like bus drivers and aircraft pilots, didn’t seem to experience a similar advantage.
    Researchers believe the association between navigation-heavy work and lower Alzheimer’s risk centers on the hippocampus, a part of the brain that governs memory and spatial navigation. It’s one of the first brain regions that Alzheimer’s damages: Problems with spatial navigation and orientation are among the earliest signs of the disease, sometimes surfacing before obvious memory loss.
    In one landmark 2000 study [link above], neuroscientists compared the brains of licensed London taxi drivers with those of people who did not drive cabs. Their findings provided the first evidence via structural imaging that regions of the adult brain can measurably change under sustained navigational demand. To earn a license, London cabbies must memorize more than 25,000 streets within a 6-mile radius of Charing Cross, a challenge known as “The Knowledge” that takes three to four years…”
    #spatialnavigation #orientation #mental #acuity #taxi #ambulance #paramedic #TheKnowledge #London #UK #Alzheimer #mapping #mentalmaps #spatialmapping #navigation #spatialreasoning #brain #hippocampus #brainhealth #death #mortality #disease #publichealth #scans #occupation #job

  34. Taxi Drivers Rarely Die Of Alzheimer’s – How Complex Mental Maps And Spatial Reasoning Protect Your Brain [why knowing your way around might help you stay sharp]
    --
    theconversation.com/taxi-drive <-- shared technical article
    --
    doi.org/10.1136/bmj-2024-082194 <-- shared paper
    --
    doi.org/10.1073/pnas.070039597 <-- shared paper
    --
    doi.org/10.1038/s41582-018-003 <-- shared paper
    --
    tfl.gov.uk/info-for/taxis-and- <-- details of @Transport for London’s ‘The Knowledge’ details
    --
    youtu.be/u7gp8KBP7ak?si=X1xXcy <-- shared video, ‘The People Who Have To Remember 25,000 Streets | The [London] Knowledge - The World's Toughest Taxi Test’
    --
    H/T @ Jennifer Psillas, GISP | GIS Project Manager at City of Tucson Parks and Recreation
    “Taxi and ambulance drivers are less likely than workers in almost any other job to die of Alzheimer’s disease. That was the surprising result of a 2024 study examining the death certificates of nearly 9 million people in the U.S…
    Of the 9 million death certificates from January 2020 to December 2022 that researchers examined, taxi and ambulance drivers had the lowest risk of dying from Alzheimer’s disease out of 443 occupations. After adjusting for age, sex, race, ethnicity and education, roughly 1 in 100 taxi and ambulance drivers died of Alzheimer’s, compared with 1 in 60 people overall.
    This pattern did not extend to other driving jobs. The researchers concluded that the key to reducing the risk of Alzheimer’s was not driving itself but continuous real-time navigation: the constant work of locating yourself in space, tracking a destination and updating a mental map as conditions change. Drivers whose jobs relied on fixed or predetermined routes, like bus drivers and aircraft pilots, didn’t seem to experience a similar advantage.
    Researchers believe the association between navigation-heavy work and lower Alzheimer’s risk centers on the hippocampus, a part of the brain that governs memory and spatial navigation. It’s one of the first brain regions that Alzheimer’s damages: Problems with spatial navigation and orientation are among the earliest signs of the disease, sometimes surfacing before obvious memory loss.
    In one landmark 2000 study [link above], neuroscientists compared the brains of licensed London taxi drivers with those of people who did not drive cabs. Their findings provided the first evidence via structural imaging that regions of the adult brain can measurably change under sustained navigational demand. To earn a license, London cabbies must memorize more than 25,000 streets within a 6-mile radius of Charing Cross, a challenge known as “The Knowledge” that takes three to four years…”
    #spatialnavigation #orientation #mental #acuity #taxi #ambulance #paramedic #TheKnowledge #London #UK #Alzheimer #mapping #mentalmaps #spatialmapping #navigation #spatialreasoning #brain #hippocampus #brainhealth #death #mortality #disease #publichealth #scans #occupation #job

  35. Taxi Drivers Rarely Die Of Alzheimer’s – How Complex Mental Maps And Spatial Reasoning Protect Your Brain [why knowing your way around might help you stay sharp]
    --
    theconversation.com/taxi-drive <-- shared technical article
    --
    doi.org/10.1136/bmj-2024-082194 <-- shared paper
    --
    doi.org/10.1073/pnas.070039597 <-- shared paper
    --
    doi.org/10.1038/s41582-018-003 <-- shared paper
    --
    tfl.gov.uk/info-for/taxis-and- <-- details of @Transport for London’s ‘The Knowledge’ details
    --
    youtu.be/u7gp8KBP7ak?si=X1xXcy <-- shared video, ‘The People Who Have To Remember 25,000 Streets | The [London] Knowledge - The World's Toughest Taxi Test’
    --
    H/T @ Jennifer Psillas, GISP | GIS Project Manager at City of Tucson Parks and Recreation
    “Taxi and ambulance drivers are less likely than workers in almost any other job to die of Alzheimer’s disease. That was the surprising result of a 2024 study examining the death certificates of nearly 9 million people in the U.S…
    Of the 9 million death certificates from January 2020 to December 2022 that researchers examined, taxi and ambulance drivers had the lowest risk of dying from Alzheimer’s disease out of 443 occupations. After adjusting for age, sex, race, ethnicity and education, roughly 1 in 100 taxi and ambulance drivers died of Alzheimer’s, compared with 1 in 60 people overall.
    This pattern did not extend to other driving jobs. The researchers concluded that the key to reducing the risk of Alzheimer’s was not driving itself but continuous real-time navigation: the constant work of locating yourself in space, tracking a destination and updating a mental map as conditions change. Drivers whose jobs relied on fixed or predetermined routes, like bus drivers and aircraft pilots, didn’t seem to experience a similar advantage.
    Researchers believe the association between navigation-heavy work and lower Alzheimer’s risk centers on the hippocampus, a part of the brain that governs memory and spatial navigation. It’s one of the first brain regions that Alzheimer’s damages: Problems with spatial navigation and orientation are among the earliest signs of the disease, sometimes surfacing before obvious memory loss.
    In one landmark 2000 study [link above], neuroscientists compared the brains of licensed London taxi drivers with those of people who did not drive cabs. Their findings provided the first evidence via structural imaging that regions of the adult brain can measurably change under sustained navigational demand. To earn a license, London cabbies must memorize more than 25,000 streets within a 6-mile radius of Charing Cross, a challenge known as “The Knowledge” that takes three to four years…”
    #spatialnavigation #orientation #mental #acuity #taxi #ambulance #paramedic #TheKnowledge #London #UK #Alzheimer #mapping #mentalmaps #spatialmapping #navigation #spatialreasoning #brain #hippocampus #brainhealth #death #mortality #disease #publichealth #scans #occupation #job

  36. Taxi Drivers Rarely Die Of Alzheimer’s – How Complex Mental Maps And Spatial Reasoning Protect Your Brain [why knowing your way around might help you stay sharp]
    --
    theconversation.com/taxi-drive <-- shared technical article
    --
    doi.org/10.1136/bmj-2024-082194 <-- shared paper
    --
    doi.org/10.1073/pnas.070039597 <-- shared paper
    --
    doi.org/10.1038/s41582-018-003 <-- shared paper
    --
    tfl.gov.uk/info-for/taxis-and- <-- details of @Transport for London’s ‘The Knowledge’ details
    --
    youtu.be/u7gp8KBP7ak?si=X1xXcy <-- shared video, ‘The People Who Have To Remember 25,000 Streets | The [London] Knowledge - The World's Toughest Taxi Test’
    --
    H/T @ Jennifer Psillas, GISP | GIS Project Manager at City of Tucson Parks and Recreation
    “Taxi and ambulance drivers are less likely than workers in almost any other job to die of Alzheimer’s disease. That was the surprising result of a 2024 study examining the death certificates of nearly 9 million people in the U.S…
    Of the 9 million death certificates from January 2020 to December 2022 that researchers examined, taxi and ambulance drivers had the lowest risk of dying from Alzheimer’s disease out of 443 occupations. After adjusting for age, sex, race, ethnicity and education, roughly 1 in 100 taxi and ambulance drivers died of Alzheimer’s, compared with 1 in 60 people overall.
    This pattern did not extend to other driving jobs. The researchers concluded that the key to reducing the risk of Alzheimer’s was not driving itself but continuous real-time navigation: the constant work of locating yourself in space, tracking a destination and updating a mental map as conditions change. Drivers whose jobs relied on fixed or predetermined routes, like bus drivers and aircraft pilots, didn’t seem to experience a similar advantage.
    Researchers believe the association between navigation-heavy work and lower Alzheimer’s risk centers on the hippocampus, a part of the brain that governs memory and spatial navigation. It’s one of the first brain regions that Alzheimer’s damages: Problems with spatial navigation and orientation are among the earliest signs of the disease, sometimes surfacing before obvious memory loss.
    In one landmark 2000 study [link above], neuroscientists compared the brains of licensed London taxi drivers with those of people who did not drive cabs. Their findings provided the first evidence via structural imaging that regions of the adult brain can measurably change under sustained navigational demand. To earn a license, London cabbies must memorize more than 25,000 streets within a 6-mile radius of Charing Cross, a challenge known as “The Knowledge” that takes three to four years…”

  37. To any #Hippocampus researchers out there:
    "representational drift" - is it good or bad?

    In the early #PlaceCells days, we would have said a neuron is not a place cell if it's not stable with time.
    Now, drift is often interpreted as a marker of "temporal coding" or "flexibility".
    What do you think?

    #RepresentationalDrift #PlaceCells #Neuroscience

  38. To any #Hippocampus researchers out there:
    "representational drift" - is it good or bad?

    In the early #PlaceCells days, we would have said a neuron is not a place cell if it's not stable with time.
    Now, drift is often interpreted as a marker of "temporal coding" or "flexibility".
    What do you think?

    #RepresentationalDrift #PlaceCells #Neuroscience

  39. To any #Hippocampus researchers out there:
    "representational drift" - is it good or bad?

    In the early #PlaceCells days, we would have said a neuron is not a place cell if it's not stable with time.
    Now, drift is often interpreted as a marker of "temporal coding" or "flexibility".
    What do you think?

    #RepresentationalDrift #PlaceCells #Neuroscience

  40. To any #Hippocampus researchers out there:
    "representational drift" - is it good or bad?

    In the early #PlaceCells days, we would have said a neuron is not a place cell if it's not stable with time.
    Now, drift is often interpreted as a marker of "temporal coding" or "flexibility".
    What do you think?

    #RepresentationalDrift #PlaceCells #Neuroscience

  41. To any #Hippocampus researchers out there:
    "representational drift" - is it good or bad?

    In the early #PlaceCells days, we would have said a neuron is not a place cell if it's not stable with time.
    Now, drift is often interpreted as a marker of "temporal coding" or "flexibility".
    What do you think?

    #RepresentationalDrift #PlaceCells #Neuroscience