#neurobiology — Public Fediverse posts
Live and recent posts from across the Fediverse tagged #neurobiology, aggregated by home.social.
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Somatostatin is a hormone traditionally recognized as a global "system manager" for growth and metabolism, but recent research reveals it primarily functions by regulating a single sleep-active neuron. This localized sleep control mechanism subsequently governs broader physiological processes across the body, including metabolism, memory consolidation, and overall lifespan.
#Neurobiology #MolecularBiology #Endocrinology #sflorg
https://www.sflorg.com/2026/05/ns05192601.html -
DATE: May 18, 2026 at 08:00PM
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: Scientists discover that dopamine receptors act as traffic signals to guide migrating brain cells
The assembly of a healthy brain requires new cells to travel incredibly long distances to arrive at their correct final destinations. A recent laboratory mouse study reveals that dopamine receptors located on stationary support cells act remarkably like traffic signals, slowing down migrating neurons so they settle in the correct areas. These findings, published in the European Journal of Neuroscience, suggest that early disruptions to dopamine signaling could permanently alter brain wiring and network connectivity.
Lead investigator Anne-Gaëlle Toutain, a neurobiology researcher at the Fer à Moulin Institute in Paris, conducted the study alongside corresponding author Christine Métin and several other academic collaborators. The team focused their efforts on analyzing the cerebral cortex, the wrinkled outer blanket of the brain responsible for higher cognitive functions. The cellular makeup of this cortical region must be perfectly balanced for the brain as a whole to function properly.
Most individual cells in the cortex are excitatory neurons, which routinely send active signaling impulses to other parts of the mammalian brain. To prevent the brain from becoming hyperactive or overwhelmed, the cortex also heavily relies on inhibitory cells known as interneurons. These smaller interneurons act as a vital cellular braking system, periodically releasing chemicals that calm overall network activity.
Excitatory neurons are born locally in the developing cortex, but the inhibitory interneurons face a much harder and more demanding physical journey. They originally emerge deep inside the core of the embryonic brain in a structure known to developmental biologists as the medial ganglionic eminence. From there, they must migrate great distances outward and upward to populate the developing outer cortex.
Neuroscientists have recognized for years that this brain cell migration is a highly choreographed and delicate biological process. To arrive safely at the correct destination, migrating interneurons must continuously read chemical cues dispersed across their cellular environment. Among these developmental cues is dopamine, a common brain chemical mostly famous for driving feelings of reward and motivation in adult brains.
Biologists possess evidence showing that dopamine is actually present very early in fetal development, arising long before the brain is fully wired or functional. Developing embryonic cells detect this chemical using specific surface proteins commonly called D1 dopamine receptors. Toutain and her entire research team wanted to find out exactly how these sensory receptors physically guide the long-distance journey of migrating interneurons.
Research into fetal dopamine signaling carries a wide range of tangible public health implications. For instance, human babies exposed to illicit drugs like cocaine in the womb fairly often suffer from smaller head sizes and a heightened biological risk of seizures. Because addictive substances directly bombard the dopamine system, they alter the delicate chemical balance needed to correctly wire the vulnerable embryonic brain.
To accurately map the cellular terrain, the researchers engineered laboratory mice to produce a glowing fluorescent protein wherever a D1 receptor was actively operating. This built-in visual marker allowed the scientists to directly map the precise physical locations of the dopamine-sensing cells in the fetal brain. They quickly observed a strangely heavy concentration of D1 receptors clustered tight in the deepest layers of the newly developing cortex.
These unique receptor-heavy cells formed a noticeably dense, continuous cellular layer right along the physical path that the migrating interneurons usually take toward the surface. The team also used analytical chemistry techniques to quantitatively confirm that raw dopamine was floating freely in these exact regions. This verified that the deeply layered cortical cells were actively responding to the chemical while the interneurons traveled aggressively past them.
To see precisely how the D1 receptor influences this cellular movement, the researchers set up isolated cell cultures in flat laboratory dishes. They extracted migrating interneurons and placed them on top of an artificial base layer composed entirely of stationary cortex cells. The research team also deployed highly targeted genetic tools to selectively delete the D1 receptor from the different tissues before ultimately combining them.
This mixing and matching allowed the researchers to watch exactly what happened when the receptor was entirely missing from the migrating cell, the stationary cell, or both cells simultaneously. They tracked the tiny movements of the cells over twenty consecutive hours using advanced time-lapse video microscopy. The resulting footage of this specific biological experiment defied initial scientific expectations about how the brain cells normally behave.
Genetically removing the D1 receptor from the migrating interneurons themselves barely changed their typical travel habits. However, when the researchers deleted the sensory receptor from the stationary cortex cells, the migrating interneurons suddenly began moving at incredibly fast speeds. The migrating cells took noticeably shorter rest pauses and dashed rapidly forward with much greater frequency than their completely unmodified counterparts.
This type of strange phenomenon is known in developmental biology as a non-cell-autonomous effect. A specific genetic alteration in one individual support cell essentially dictates the physical movement behavior of a completely different brain cell. The active D1 receptors on the stationary cortex cells normally act exactly like a textured terrain, heavily slowing down the migrating neurons to a far more manageable physiological pace.
To see if this fast-paced embryonic migration permanently altered the functional anatomy of the brain, the team closely examined fully grown adult mice. They engineered a dedicated group of test mice to lack D1 receptors exclusively in their stationary cortex cells. Because the migrating interneurons in these mice retained completely normal genetics, any subsequent structural changes would absolutely have to stem from the altered cellular terrain.
The researchers counted two distinct biological populations of interneurons to see where they eventually settled across the mature brain. One population consisted of somatostatin-producing cells, which usually migrate very early in the general timeline of embryonic development. The other group was made up of parvalbumin-producing cells, which generally migrate a few days later in the normal fetal maturation schedule.
Because they moved entirely too fast across the slippery cellular terrain, both subsets of cells severely overshot their originally intended marks. The early somatostatin cells piled up in abnormally high numbers at the extreme front and middle edges of the fully formed cortex. The later parvalbumin cells essentially accumulated in the dense sensory regions at the remote back of the completed brain.
Finally, the researchers evaluated mice missing the key D1 receptor entirely, possessing genetic instructions where absolutely no cells in their bodies could ever detect targeted dopamine signals. This profound genetic model closely resembles the biological reality of a severe organism-wide mutation. Without the primary D1 receptor guiding early cortical growth, the overall physical volume of the cerebral cortex shrank dramatically by roughly a full quarter.
Despite experiencing this massive reduction in total brain volume, the interneurons still clustered in the exact same abnormal architectural patterns at the outer edges of the cortex. This conclusive phase of the study showed that the physical environment created by the cortex cells overwhelmingly dominates the cellular migration process. Even in a stunted biological brain, the missing cellular speed bumps sent the migrating cells flying blindly toward the outermost boundaries.
There are still a few missing experimental pieces to this fascinating neurobiological puzzle. The exact biological mechanism that the stationary cortex cells use to slow down the sweeping interneurons remains unknown to the scientific community at large. The active dopamine receptors might alter the overall physical shape of the support cells, or they might subtly change how sticky or slippery the cellular surfaces eventually become.
Future researchers will definitively need to untangle the hidden physical and chemical interactions occurring at the exact microscopic locations where these two cell types frequently touch. Uncovering these hidden mechanisms could eventually shed bright light on a wide variety of poorly understood developmental disorders. Unusually high or low densities of local interneurons are an established feature in the brains of some patients diagnosed medically with schizophrenia and autism.
If fetal dopamine signaling becomes disturbed by inherited genetic traits or external environmental factors, it could eventually lead to these permanent, lifelong structural shifts. The latest findings illustrate how such a seemingly tiny molecular event can ripple outward to reshape the entire physical brain architecture. Understanding this early cellular journey acts as a foundational jumping-off point toward ultimately treating broader neurodevelopmental disorders down the line.
The study, “Ablation of the D1 Dopamine Receptor Alters the Migration and the Cortical Distribution of MGE-Derived Inhibitory Interneurons by a Preponderant Non–Cell-Autonomous Effect,” was authored by Anne-Gaëlle Toutain, Sophie Scotto-Lomassese, Aude Muzerelle, Julien Puech, Ariane Fayad, Anne Roumier, Denis Hervé, and Christine Métin.
-------------------------------------------------
DAILY EMAIL DIGEST: Email [email protected] -- no subject or message needed.
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
NYU Information for Practice puts out 400-500 good quality health-related research posts per week but its too much for many people, so that bot is limited to just subscribers. You can read it or subscribe at @PsychResearchBot
Since 1991 The National Psychologist has focused on keeping practicing psychologists current with news, information and items of interest. Check them out for more free articles, resources, and subscription information: https://www.nationalpsychologist.com
EMAIL DAILY DIGEST OF RSS FEEDS -- SUBSCRIBE: http://subscribe-article-digests.clinicians-exchange.org
READ ONLINE: http://read-the-rss-mega-archive.clinicians-exchange.org
It's primitive... but it works... mostly...
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #DopamineSignals #InterneuronsMigration #CorticalDevelopment #D1Receptors #Neurobiology #BrainWiring #NonCellAutonomous #NeuroscienceResearch #NeuroDevelopment #BrainConnectivity
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DATE: May 18, 2026 at 08:00PM
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: Scientists discover that dopamine receptors act as traffic signals to guide migrating brain cells
The assembly of a healthy brain requires new cells to travel incredibly long distances to arrive at their correct final destinations. A recent laboratory mouse study reveals that dopamine receptors located on stationary support cells act remarkably like traffic signals, slowing down migrating neurons so they settle in the correct areas. These findings, published in the European Journal of Neuroscience, suggest that early disruptions to dopamine signaling could permanently alter brain wiring and network connectivity.
Lead investigator Anne-Gaëlle Toutain, a neurobiology researcher at the Fer à Moulin Institute in Paris, conducted the study alongside corresponding author Christine Métin and several other academic collaborators. The team focused their efforts on analyzing the cerebral cortex, the wrinkled outer blanket of the brain responsible for higher cognitive functions. The cellular makeup of this cortical region must be perfectly balanced for the brain as a whole to function properly.
Most individual cells in the cortex are excitatory neurons, which routinely send active signaling impulses to other parts of the mammalian brain. To prevent the brain from becoming hyperactive or overwhelmed, the cortex also heavily relies on inhibitory cells known as interneurons. These smaller interneurons act as a vital cellular braking system, periodically releasing chemicals that calm overall network activity.
Excitatory neurons are born locally in the developing cortex, but the inhibitory interneurons face a much harder and more demanding physical journey. They originally emerge deep inside the core of the embryonic brain in a structure known to developmental biologists as the medial ganglionic eminence. From there, they must migrate great distances outward and upward to populate the developing outer cortex.
Neuroscientists have recognized for years that this brain cell migration is a highly choreographed and delicate biological process. To arrive safely at the correct destination, migrating interneurons must continuously read chemical cues dispersed across their cellular environment. Among these developmental cues is dopamine, a common brain chemical mostly famous for driving feelings of reward and motivation in adult brains.
Biologists possess evidence showing that dopamine is actually present very early in fetal development, arising long before the brain is fully wired or functional. Developing embryonic cells detect this chemical using specific surface proteins commonly called D1 dopamine receptors. Toutain and her entire research team wanted to find out exactly how these sensory receptors physically guide the long-distance journey of migrating interneurons.
Research into fetal dopamine signaling carries a wide range of tangible public health implications. For instance, human babies exposed to illicit drugs like cocaine in the womb fairly often suffer from smaller head sizes and a heightened biological risk of seizures. Because addictive substances directly bombard the dopamine system, they alter the delicate chemical balance needed to correctly wire the vulnerable embryonic brain.
To accurately map the cellular terrain, the researchers engineered laboratory mice to produce a glowing fluorescent protein wherever a D1 receptor was actively operating. This built-in visual marker allowed the scientists to directly map the precise physical locations of the dopamine-sensing cells in the fetal brain. They quickly observed a strangely heavy concentration of D1 receptors clustered tight in the deepest layers of the newly developing cortex.
These unique receptor-heavy cells formed a noticeably dense, continuous cellular layer right along the physical path that the migrating interneurons usually take toward the surface. The team also used analytical chemistry techniques to quantitatively confirm that raw dopamine was floating freely in these exact regions. This verified that the deeply layered cortical cells were actively responding to the chemical while the interneurons traveled aggressively past them.
To see precisely how the D1 receptor influences this cellular movement, the researchers set up isolated cell cultures in flat laboratory dishes. They extracted migrating interneurons and placed them on top of an artificial base layer composed entirely of stationary cortex cells. The research team also deployed highly targeted genetic tools to selectively delete the D1 receptor from the different tissues before ultimately combining them.
This mixing and matching allowed the researchers to watch exactly what happened when the receptor was entirely missing from the migrating cell, the stationary cell, or both cells simultaneously. They tracked the tiny movements of the cells over twenty consecutive hours using advanced time-lapse video microscopy. The resulting footage of this specific biological experiment defied initial scientific expectations about how the brain cells normally behave.
Genetically removing the D1 receptor from the migrating interneurons themselves barely changed their typical travel habits. However, when the researchers deleted the sensory receptor from the stationary cortex cells, the migrating interneurons suddenly began moving at incredibly fast speeds. The migrating cells took noticeably shorter rest pauses and dashed rapidly forward with much greater frequency than their completely unmodified counterparts.
This type of strange phenomenon is known in developmental biology as a non-cell-autonomous effect. A specific genetic alteration in one individual support cell essentially dictates the physical movement behavior of a completely different brain cell. The active D1 receptors on the stationary cortex cells normally act exactly like a textured terrain, heavily slowing down the migrating neurons to a far more manageable physiological pace.
To see if this fast-paced embryonic migration permanently altered the functional anatomy of the brain, the team closely examined fully grown adult mice. They engineered a dedicated group of test mice to lack D1 receptors exclusively in their stationary cortex cells. Because the migrating interneurons in these mice retained completely normal genetics, any subsequent structural changes would absolutely have to stem from the altered cellular terrain.
The researchers counted two distinct biological populations of interneurons to see where they eventually settled across the mature brain. One population consisted of somatostatin-producing cells, which usually migrate very early in the general timeline of embryonic development. The other group was made up of parvalbumin-producing cells, which generally migrate a few days later in the normal fetal maturation schedule.
Because they moved entirely too fast across the slippery cellular terrain, both subsets of cells severely overshot their originally intended marks. The early somatostatin cells piled up in abnormally high numbers at the extreme front and middle edges of the fully formed cortex. The later parvalbumin cells essentially accumulated in the dense sensory regions at the remote back of the completed brain.
Finally, the researchers evaluated mice missing the key D1 receptor entirely, possessing genetic instructions where absolutely no cells in their bodies could ever detect targeted dopamine signals. This profound genetic model closely resembles the biological reality of a severe organism-wide mutation. Without the primary D1 receptor guiding early cortical growth, the overall physical volume of the cerebral cortex shrank dramatically by roughly a full quarter.
Despite experiencing this massive reduction in total brain volume, the interneurons still clustered in the exact same abnormal architectural patterns at the outer edges of the cortex. This conclusive phase of the study showed that the physical environment created by the cortex cells overwhelmingly dominates the cellular migration process. Even in a stunted biological brain, the missing cellular speed bumps sent the migrating cells flying blindly toward the outermost boundaries.
There are still a few missing experimental pieces to this fascinating neurobiological puzzle. The exact biological mechanism that the stationary cortex cells use to slow down the sweeping interneurons remains unknown to the scientific community at large. The active dopamine receptors might alter the overall physical shape of the support cells, or they might subtly change how sticky or slippery the cellular surfaces eventually become.
Future researchers will definitively need to untangle the hidden physical and chemical interactions occurring at the exact microscopic locations where these two cell types frequently touch. Uncovering these hidden mechanisms could eventually shed bright light on a wide variety of poorly understood developmental disorders. Unusually high or low densities of local interneurons are an established feature in the brains of some patients diagnosed medically with schizophrenia and autism.
If fetal dopamine signaling becomes disturbed by inherited genetic traits or external environmental factors, it could eventually lead to these permanent, lifelong structural shifts. The latest findings illustrate how such a seemingly tiny molecular event can ripple outward to reshape the entire physical brain architecture. Understanding this early cellular journey acts as a foundational jumping-off point toward ultimately treating broader neurodevelopmental disorders down the line.
The study, “Ablation of the D1 Dopamine Receptor Alters the Migration and the Cortical Distribution of MGE-Derived Inhibitory Interneurons by a Preponderant Non–Cell-Autonomous Effect,” was authored by Anne-Gaëlle Toutain, Sophie Scotto-Lomassese, Aude Muzerelle, Julien Puech, Ariane Fayad, Anne Roumier, Denis Hervé, and Christine Métin.
-------------------------------------------------
DAILY EMAIL DIGEST: Email [email protected] -- no subject or message needed.
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
NYU Information for Practice puts out 400-500 good quality health-related research posts per week but its too much for many people, so that bot is limited to just subscribers. You can read it or subscribe at @PsychResearchBot
Since 1991 The National Psychologist has focused on keeping practicing psychologists current with news, information and items of interest. Check them out for more free articles, resources, and subscription information: https://www.nationalpsychologist.com
EMAIL DAILY DIGEST OF RSS FEEDS -- SUBSCRIBE: http://subscribe-article-digests.clinicians-exchange.org
READ ONLINE: http://read-the-rss-mega-archive.clinicians-exchange.org
It's primitive... but it works... mostly...
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #DopamineSignals #InterneuronsMigration #CorticalDevelopment #D1Receptors #Neurobiology #BrainWiring #NonCellAutonomous #NeuroscienceResearch #NeuroDevelopment #BrainConnectivity
-
DATE: May 18, 2026 at 08:00PM
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: Scientists discover that dopamine receptors act as traffic signals to guide migrating brain cells
The assembly of a healthy brain requires new cells to travel incredibly long distances to arrive at their correct final destinations. A recent laboratory mouse study reveals that dopamine receptors located on stationary support cells act remarkably like traffic signals, slowing down migrating neurons so they settle in the correct areas. These findings, published in the European Journal of Neuroscience, suggest that early disruptions to dopamine signaling could permanently alter brain wiring and network connectivity.
Lead investigator Anne-Gaëlle Toutain, a neurobiology researcher at the Fer à Moulin Institute in Paris, conducted the study alongside corresponding author Christine Métin and several other academic collaborators. The team focused their efforts on analyzing the cerebral cortex, the wrinkled outer blanket of the brain responsible for higher cognitive functions. The cellular makeup of this cortical region must be perfectly balanced for the brain as a whole to function properly.
Most individual cells in the cortex are excitatory neurons, which routinely send active signaling impulses to other parts of the mammalian brain. To prevent the brain from becoming hyperactive or overwhelmed, the cortex also heavily relies on inhibitory cells known as interneurons. These smaller interneurons act as a vital cellular braking system, periodically releasing chemicals that calm overall network activity.
Excitatory neurons are born locally in the developing cortex, but the inhibitory interneurons face a much harder and more demanding physical journey. They originally emerge deep inside the core of the embryonic brain in a structure known to developmental biologists as the medial ganglionic eminence. From there, they must migrate great distances outward and upward to populate the developing outer cortex.
Neuroscientists have recognized for years that this brain cell migration is a highly choreographed and delicate biological process. To arrive safely at the correct destination, migrating interneurons must continuously read chemical cues dispersed across their cellular environment. Among these developmental cues is dopamine, a common brain chemical mostly famous for driving feelings of reward and motivation in adult brains.
Biologists possess evidence showing that dopamine is actually present very early in fetal development, arising long before the brain is fully wired or functional. Developing embryonic cells detect this chemical using specific surface proteins commonly called D1 dopamine receptors. Toutain and her entire research team wanted to find out exactly how these sensory receptors physically guide the long-distance journey of migrating interneurons.
Research into fetal dopamine signaling carries a wide range of tangible public health implications. For instance, human babies exposed to illicit drugs like cocaine in the womb fairly often suffer from smaller head sizes and a heightened biological risk of seizures. Because addictive substances directly bombard the dopamine system, they alter the delicate chemical balance needed to correctly wire the vulnerable embryonic brain.
To accurately map the cellular terrain, the researchers engineered laboratory mice to produce a glowing fluorescent protein wherever a D1 receptor was actively operating. This built-in visual marker allowed the scientists to directly map the precise physical locations of the dopamine-sensing cells in the fetal brain. They quickly observed a strangely heavy concentration of D1 receptors clustered tight in the deepest layers of the newly developing cortex.
These unique receptor-heavy cells formed a noticeably dense, continuous cellular layer right along the physical path that the migrating interneurons usually take toward the surface. The team also used analytical chemistry techniques to quantitatively confirm that raw dopamine was floating freely in these exact regions. This verified that the deeply layered cortical cells were actively responding to the chemical while the interneurons traveled aggressively past them.
To see precisely how the D1 receptor influences this cellular movement, the researchers set up isolated cell cultures in flat laboratory dishes. They extracted migrating interneurons and placed them on top of an artificial base layer composed entirely of stationary cortex cells. The research team also deployed highly targeted genetic tools to selectively delete the D1 receptor from the different tissues before ultimately combining them.
This mixing and matching allowed the researchers to watch exactly what happened when the receptor was entirely missing from the migrating cell, the stationary cell, or both cells simultaneously. They tracked the tiny movements of the cells over twenty consecutive hours using advanced time-lapse video microscopy. The resulting footage of this specific biological experiment defied initial scientific expectations about how the brain cells normally behave.
Genetically removing the D1 receptor from the migrating interneurons themselves barely changed their typical travel habits. However, when the researchers deleted the sensory receptor from the stationary cortex cells, the migrating interneurons suddenly began moving at incredibly fast speeds. The migrating cells took noticeably shorter rest pauses and dashed rapidly forward with much greater frequency than their completely unmodified counterparts.
This type of strange phenomenon is known in developmental biology as a non-cell-autonomous effect. A specific genetic alteration in one individual support cell essentially dictates the physical movement behavior of a completely different brain cell. The active D1 receptors on the stationary cortex cells normally act exactly like a textured terrain, heavily slowing down the migrating neurons to a far more manageable physiological pace.
To see if this fast-paced embryonic migration permanently altered the functional anatomy of the brain, the team closely examined fully grown adult mice. They engineered a dedicated group of test mice to lack D1 receptors exclusively in their stationary cortex cells. Because the migrating interneurons in these mice retained completely normal genetics, any subsequent structural changes would absolutely have to stem from the altered cellular terrain.
The researchers counted two distinct biological populations of interneurons to see where they eventually settled across the mature brain. One population consisted of somatostatin-producing cells, which usually migrate very early in the general timeline of embryonic development. The other group was made up of parvalbumin-producing cells, which generally migrate a few days later in the normal fetal maturation schedule.
Because they moved entirely too fast across the slippery cellular terrain, both subsets of cells severely overshot their originally intended marks. The early somatostatin cells piled up in abnormally high numbers at the extreme front and middle edges of the fully formed cortex. The later parvalbumin cells essentially accumulated in the dense sensory regions at the remote back of the completed brain.
Finally, the researchers evaluated mice missing the key D1 receptor entirely, possessing genetic instructions where absolutely no cells in their bodies could ever detect targeted dopamine signals. This profound genetic model closely resembles the biological reality of a severe organism-wide mutation. Without the primary D1 receptor guiding early cortical growth, the overall physical volume of the cerebral cortex shrank dramatically by roughly a full quarter.
Despite experiencing this massive reduction in total brain volume, the interneurons still clustered in the exact same abnormal architectural patterns at the outer edges of the cortex. This conclusive phase of the study showed that the physical environment created by the cortex cells overwhelmingly dominates the cellular migration process. Even in a stunted biological brain, the missing cellular speed bumps sent the migrating cells flying blindly toward the outermost boundaries.
There are still a few missing experimental pieces to this fascinating neurobiological puzzle. The exact biological mechanism that the stationary cortex cells use to slow down the sweeping interneurons remains unknown to the scientific community at large. The active dopamine receptors might alter the overall physical shape of the support cells, or they might subtly change how sticky or slippery the cellular surfaces eventually become.
Future researchers will definitively need to untangle the hidden physical and chemical interactions occurring at the exact microscopic locations where these two cell types frequently touch. Uncovering these hidden mechanisms could eventually shed bright light on a wide variety of poorly understood developmental disorders. Unusually high or low densities of local interneurons are an established feature in the brains of some patients diagnosed medically with schizophrenia and autism.
If fetal dopamine signaling becomes disturbed by inherited genetic traits or external environmental factors, it could eventually lead to these permanent, lifelong structural shifts. The latest findings illustrate how such a seemingly tiny molecular event can ripple outward to reshape the entire physical brain architecture. Understanding this early cellular journey acts as a foundational jumping-off point toward ultimately treating broader neurodevelopmental disorders down the line.
The study, “Ablation of the D1 Dopamine Receptor Alters the Migration and the Cortical Distribution of MGE-Derived Inhibitory Interneurons by a Preponderant Non–Cell-Autonomous Effect,” was authored by Anne-Gaëlle Toutain, Sophie Scotto-Lomassese, Aude Muzerelle, Julien Puech, Ariane Fayad, Anne Roumier, Denis Hervé, and Christine Métin.
-------------------------------------------------
DAILY EMAIL DIGEST: Email [email protected] -- no subject or message needed.
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
NYU Information for Practice puts out 400-500 good quality health-related research posts per week but its too much for many people, so that bot is limited to just subscribers. You can read it or subscribe at @PsychResearchBot
Since 1991 The National Psychologist has focused on keeping practicing psychologists current with news, information and items of interest. Check them out for more free articles, resources, and subscription information: https://www.nationalpsychologist.com
EMAIL DAILY DIGEST OF RSS FEEDS -- SUBSCRIBE: http://subscribe-article-digests.clinicians-exchange.org
READ ONLINE: http://read-the-rss-mega-archive.clinicians-exchange.org
It's primitive... but it works... mostly...
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #DopamineSignals #InterneuronsMigration #CorticalDevelopment #D1Receptors #Neurobiology #BrainWiring #NonCellAutonomous #NeuroscienceResearch #NeuroDevelopment #BrainConnectivity
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Despite their role in highly complex brain networks, individual neurons primarily operate as simple on-off switches governed by basic, one-input-to-one-output interactions.
#Biophysics #ComputationalNeuroscience #Neurobiology #sflorg
https://www.sflorg.com/2026/05/biph05182601.html -
Overall Brain Health Protects Memory From Early Alzheimer’s
Summary: A collaborative study reveals that maintaining robust overall brain health can protect memory and thinking skills from…
#NewsBeep #News #Health #aging #Alzheimer'sdisease #brainhealth #brainresearch #cognitivereserve #dementia #GB #Memory #murdochuniversity #neurobiology #neurodegenerativedisease #Neurology #Neuroscience #UK #UnitedKingdom
https://www.newsbeep.com/uk/589402/ -
Overall Brain Health Protects Memory From Early Alzheimer’s
Summary: A collaborative study reveals that maintaining robust overall brain health can protect memory and thinking skills from…
#NewsBeep #News #US #USA #UnitedStates #UnitedStatesOfAmerica #Health #aging #Alzheimer'sdisease #brainhealth #brainresearch #cognitivereserve #dementia #Memory #murdochuniversity #neurobiology #NeurodegenerativeDisease #Neurology #Neuroscience
https://www.newsbeep.com/us/648637/ -
Overall Brain Health Protects Memory From Early Alzheimer’s
Summary: A collaborative study reveals that maintaining robust overall brain health can protect memory and thinking skills from…
#NewsBeep #News #US #USA #UnitedStates #UnitedStatesOfAmerica #Health #aging #Alzheimer'sdisease #brainhealth #brainresearch #cognitivereserve #dementia #Memory #murdochuniversity #neurobiology #NeurodegenerativeDisease #Neurology #Neuroscience
https://www.newsbeep.com/us/648637/ -
Review of 60+ Alcohol-Caused Diseases Details Reversibility
Summary: A new comprehensive review reinforces the substantial toll alcohol consumption takes on global health. The research highlights…
#NewsBeep #News #US #USA #UnitedStates #UnitedStatesOfAmerica #Health #addiction #alcoholconsumption #aud #brainresearch #neurobiology #Neuroscience #Psychology #ReversibleBrainDamage #societyforthestudyofaddiction
https://www.newsbeep.com/us/646773/ -
Review of 60+ Alcohol-Caused Diseases Details Reversibility
Summary: A new comprehensive review reinforces the substantial toll alcohol consumption takes on global health. The research highlights…
#NewsBeep #News #US #USA #UnitedStates #UnitedStatesOfAmerica #Health #addiction #alcoholconsumption #aud #brainresearch #neurobiology #Neuroscience #Psychology #ReversibleBrainDamage #societyforthestudyofaddiction
https://www.newsbeep.com/us/646773/ -
Harsh Parenting Biologically Distorts Child Stress Regulation
Summary: A new study provides biological proof for how aggressive parenting alters a child’s ability to handle stress.…
#NewsBeep #News #US #USA #UnitedStates #UnitedStatesOfAmerica #Health #braindevelopment #brainresearch #developmentalneuroscience #Mentalhealth #neurobiology #neurodevelopment #Neuroscience #Parenting #PennState #Psychology #stress
https://www.newsbeep.com/us/646290/ -
Harsh Parenting Biologically Distorts Child Stress Regulation
Summary: A new study provides biological proof for how aggressive parenting alters a child’s ability to handle stress.…
#NewsBeep #News #US #USA #UnitedStates #UnitedStatesOfAmerica #Health #braindevelopment #brainresearch #developmentalneuroscience #Mentalhealth #neurobiology #neurodevelopment #Neuroscience #Parenting #PennState #Psychology #stress
https://www.newsbeep.com/us/646290/ -
Adenine base editing, a highly targeted form of genetic medicine, has been successfully deployed in a preclinical mouse model to correct the specific DNA mutation (SCN1A) responsible for Dravet syndrome, a severe and often fatal form of childhood epilepsy.
#MolecularGenetics #Neurobiology #GeneTherapy #PrecisionMedicine #sflorg
https://www.sflorg.com/2026/05/gen05142601.html -
Adenine base editing, a highly targeted form of genetic medicine, has been successfully deployed in a preclinical mouse model to correct the specific DNA mutation (SCN1A) responsible for Dravet syndrome, a severe and often fatal form of childhood epilepsy.
#MolecularGenetics #Neurobiology #GeneTherapy #PrecisionMedicine #sflorg
https://www.sflorg.com/2026/05/gen05142601.html -
Adenine base editing, a highly targeted form of genetic medicine, has been successfully deployed in a preclinical mouse model to correct the specific DNA mutation (SCN1A) responsible for Dravet syndrome, a severe and often fatal form of childhood epilepsy.
#MolecularGenetics #Neurobiology #GeneTherapy #PrecisionMedicine #sflorg
https://www.sflorg.com/2026/05/gen05142601.html -
Adenine base editing, a highly targeted form of genetic medicine, has been successfully deployed in a preclinical mouse model to correct the specific DNA mutation (SCN1A) responsible for Dravet syndrome, a severe and often fatal form of childhood epilepsy.
#MolecularGenetics #Neurobiology #GeneTherapy #PrecisionMedicine #sflorg
https://www.sflorg.com/2026/05/gen05142601.html -
Adenine base editing, a highly targeted form of genetic medicine, has been successfully deployed in a preclinical mouse model to correct the specific DNA mutation (SCN1A) responsible for Dravet syndrome, a severe and often fatal form of childhood epilepsy.
#MolecularGenetics #Neurobiology #GeneTherapy #PrecisionMedicine #sflorg
https://www.sflorg.com/2026/05/gen05142601.html -
A political or religious cult functions as a synthetic, weaponized ecosystem meticulously structured to hijack adaptive human evolutionary traits, manipulate neurochemistry, and enforce cognitive compliance through systemic biological pressure.
#WhatIs #EvolutionaryBiology #Neurobiology #BehavioralPsychology #Neuroscience #sflorg
https://www.sflorg.com/2026/05/wi05142601.html -
A political or religious cult functions as a synthetic, weaponized ecosystem meticulously structured to hijack adaptive human evolutionary traits, manipulate neurochemistry, and enforce cognitive compliance through systemic biological pressure.
#WhatIs #EvolutionaryBiology #Neurobiology #BehavioralPsychology #Neuroscience #sflorg
https://www.sflorg.com/2026/05/wi05142601.html -
A political or religious cult functions as a synthetic, weaponized ecosystem meticulously structured to hijack adaptive human evolutionary traits, manipulate neurochemistry, and enforce cognitive compliance through systemic biological pressure.
#WhatIs #EvolutionaryBiology #Neurobiology #BehavioralPsychology #Neuroscience #sflorg
https://www.sflorg.com/2026/05/wi05142601.html -
A political or religious cult functions as a synthetic, weaponized ecosystem meticulously structured to hijack adaptive human evolutionary traits, manipulate neurochemistry, and enforce cognitive compliance through systemic biological pressure.
#WhatIs #EvolutionaryBiology #Neurobiology #BehavioralPsychology #Neuroscience #sflorg
https://www.sflorg.com/2026/05/wi05142601.html -
A political or religious cult functions as a synthetic, weaponized ecosystem meticulously structured to hijack adaptive human evolutionary traits, manipulate neurochemistry, and enforce cognitive compliance through systemic biological pressure.
#WhatIs #EvolutionaryBiology #Neurobiology #BehavioralPsychology #Neuroscience #sflorg
https://www.sflorg.com/2026/05/wi05142601.html -
Anti-Nogo-A therapy utilizes a novel monoclonal antibody, NG101, to stimulate the regeneration of damaged spinal cord tissue. By neutralizing growth-inhibiting proteins in the central nervous system, it enables severed nerve pathways to re-establish functional connections.
#Neuroscience #Neurobiology #ClinicalNeurology #sflorg
https://www.sflorg.com/2026/05/ns05122601.html -
Anti-Nogo-A therapy utilizes a novel monoclonal antibody, NG101, to stimulate the regeneration of damaged spinal cord tissue. By neutralizing growth-inhibiting proteins in the central nervous system, it enables severed nerve pathways to re-establish functional connections.
#Neuroscience #Neurobiology #ClinicalNeurology #sflorg
https://www.sflorg.com/2026/05/ns05122601.html -
Anti-Nogo-A therapy utilizes a novel monoclonal antibody, NG101, to stimulate the regeneration of damaged spinal cord tissue. By neutralizing growth-inhibiting proteins in the central nervous system, it enables severed nerve pathways to re-establish functional connections.
#Neuroscience #Neurobiology #ClinicalNeurology #sflorg
https://www.sflorg.com/2026/05/ns05122601.html -
Anti-Nogo-A therapy utilizes a novel monoclonal antibody, NG101, to stimulate the regeneration of damaged spinal cord tissue. By neutralizing growth-inhibiting proteins in the central nervous system, it enables severed nerve pathways to re-establish functional connections.
#Neuroscience #Neurobiology #ClinicalNeurology #sflorg
https://www.sflorg.com/2026/05/ns05122601.html -
Anti-Nogo-A therapy utilizes a novel monoclonal antibody, NG101, to stimulate the regeneration of damaged spinal cord tissue. By neutralizing growth-inhibiting proteins in the central nervous system, it enables severed nerve pathways to re-establish functional connections.
#Neuroscience #Neurobiology #ClinicalNeurology #sflorg
https://www.sflorg.com/2026/05/ns05122601.html -
Chaperone tubulinopathies are severe, life-shortening inherited genetic disorders caused by mutations in tubulin cofactors, which are essential proteins that control the formation of a cell's microtubule skeleton. These mutations disrupt the structural development of growing neurons, leading to severe neurological and developmental defects in infants.
#MolecularBiology #CellBiology #Neurobiology #Genetics #sflorg
https://www.sflorg.com/2026/05/mbio05102601.html -
Chaperone tubulinopathies are severe, life-shortening inherited genetic disorders caused by mutations in tubulin cofactors, which are essential proteins that control the formation of a cell's microtubule skeleton. These mutations disrupt the structural development of growing neurons, leading to severe neurological and developmental defects in infants.
#MolecularBiology #CellBiology #Neurobiology #Genetics #sflorg
https://www.sflorg.com/2026/05/mbio05102601.html -
Chaperone tubulinopathies are severe, life-shortening inherited genetic disorders caused by mutations in tubulin cofactors, which are essential proteins that control the formation of a cell's microtubule skeleton. These mutations disrupt the structural development of growing neurons, leading to severe neurological and developmental defects in infants.
#MolecularBiology #CellBiology #Neurobiology #Genetics #sflorg
https://www.sflorg.com/2026/05/mbio05102601.html -
Chaperone tubulinopathies are severe, life-shortening inherited genetic disorders caused by mutations in tubulin cofactors, which are essential proteins that control the formation of a cell's microtubule skeleton. These mutations disrupt the structural development of growing neurons, leading to severe neurological and developmental defects in infants.
#MolecularBiology #CellBiology #Neurobiology #Genetics #sflorg
https://www.sflorg.com/2026/05/mbio05102601.html -
Chaperone tubulinopathies are severe, life-shortening inherited genetic disorders caused by mutations in tubulin cofactors, which are essential proteins that control the formation of a cell's microtubule skeleton. These mutations disrupt the structural development of growing neurons, leading to severe neurological and developmental defects in infants.
#MolecularBiology #CellBiology #Neurobiology #Genetics #sflorg
https://www.sflorg.com/2026/05/mbio05102601.html -
Reducing Visceral Fat Protects the Brain for Decades
Summary: A new longitudinal study reveals that the accumulation of visceral fat, the “hidden” fat stored deep within…
#NewsBeep #News #Health #aging #Ben-GurionUniversityoftheNegev #brainaging #brainatrophy #brainresearch #cognition #cognitivedecline #dementia #GB #glucosecontrol #hippocampus #insulinsensitivity #neurobiology #Neurology #Neuroscience #UK #UnitedKingdom #visceralfat
https://www.newsbeep.com/uk/576103/ -
Beyond the Gym: Why Your Brain Craves Creatine
Summary: Creatine is far more than a “gym supplement”; it is a naturally occurring compound essential for cellular…
#NewsBeep #News #Nutrition #Aging #ATPRegeneration #AU #Australia #brainenergy #brainhealth #brainresearch #cognition #cognitivefunction #creatine #dietarysupplements #Health #MuscleMetabolism #neurobiology #Neuroscience #Phosphocreatine #TaylorandFrancisGroup
https://www.newsbeep.com/au/660919/ -
Beyond the Gym: Why Your Brain Craves Creatine
Summary: Creatine is far more than a “gym supplement”; it is a naturally occurring compound essential for cellular…
#NewsBeep #News #Nutrition #Aging #ATPRegeneration #AU #Australia #brainenergy #brainhealth #brainresearch #cognition #cognitivefunction #creatine #dietarysupplements #Health #MuscleMetabolism #neurobiology #Neuroscience #Phosphocreatine #TaylorandFrancisGroup
https://www.newsbeep.com/au/660919/ -
https://www.europesays.com/ie/477120/ Beyond the Gym: Why Your Brain Craves Creatine #Aging #ATPRegeneration #BrainEnergy #BrainHealth #BrainResearch #Cognition #CognitiveFunction #creatine #DietarySupplements #Éire #Health #IE #Ireland #MuscleMetabolism #neurobiology #Neuroscience #Nutrition #Phosphocreatine #TaylorAndFrancisGroup
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https://www.europesays.com/uk/949351/ Brain Switch for Action and Stress Identified #ACC #addiction #AnteriorCingulateCortex #AutonomicArousal #BrainResearch #Health #LocusCoeruleus #neurobiology #Neurology #Neuroscience #Parkinson'sDisease #RutgersUniversity #Stress #UK #UnitedKingdom
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Brain Performance Can Improve at Any Age
Summary: A three-year longitudinal study has debunked the long-standing myth that cognitive decline is an inevitable part of…
#NewsBeep #News #Health #Aging #AU #Australia #brainhealth #brainresearch #cognition #cognitiveperformance #memory #mentalresilience #neurobiology #neuroplasticity #Neuroscience #UTDallas
https://www.newsbeep.com/au/658111/ -
Brain Performance Can Improve at Any Age
Summary: A three-year longitudinal study has debunked the long-standing myth that cognitive decline is an inevitable part of…
#NewsBeep #News #Health #Aging #AU #Australia #brainhealth #brainresearch #cognition #cognitiveperformance #memory #mentalresilience #neurobiology #neuroplasticity #Neuroscience #UTDallas
https://www.newsbeep.com/au/658111/ -
💊New approach to treating spinal cord injuries developed
A team led by Prof. Dr. Dietmar Fischer at the University Hospital Cologne demonstrated in mouse models that the engineered protein hIL‑6 induces new neuronal connections in the injured spinal cord, partially restoring lost motor function.⚠️ More research on safety, optimal dosing, and side effects is required before human application.
Read more ▶️ https://uni.koeln/KX675
#Research #SpinalCordInjury #Neuroscience #hIL6 #Neurobiology
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💊New approach to treating spinal cord injuries developed
A team led by Prof. Dr. Dietmar Fischer at the University Hospital Cologne demonstrated in mouse models that the engineered protein hIL‑6 induces new neuronal connections in the injured spinal cord, partially restoring lost motor function.⚠️ More research on safety, optimal dosing, and side effects is required before human application.
Read more ▶️ https://uni.koeln/KX675
#Research #SpinalCordInjury #Neuroscience #hIL6 #Neurobiology
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💊New approach to treating spinal cord injuries developed
A team led by Prof. Dr. Dietmar Fischer at the University Hospital Cologne demonstrated in mouse models that the engineered protein hIL‑6 induces new neuronal connections in the injured spinal cord, partially restoring lost motor function.⚠️ More research on safety, optimal dosing, and side effects is required before human application.
Read more ▶️ https://uni.koeln/KX675
#Research #SpinalCordInjury #Neuroscience #hIL6 #Neurobiology
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💊New approach to treating spinal cord injuries developed
A team led by Prof. Dr. Dietmar Fischer at the University Hospital Cologne demonstrated in mouse models that the engineered protein hIL‑6 induces new neuronal connections in the injured spinal cord, partially restoring lost motor function.⚠️ More research on safety, optimal dosing, and side effects is required before human application.
Read more ▶️ https://uni.koeln/KX675
#Research #SpinalCordInjury #Neuroscience #hIL6 #Neurobiology
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💊New approach to treating spinal cord injuries developed
A team led by Prof. Dr. Dietmar Fischer at the University Hospital Cologne demonstrated in mouse models that the engineered protein hIL‑6 induces new neuronal connections in the injured spinal cord, partially restoring lost motor function.⚠️ More research on safety, optimal dosing, and side effects is required before human application.
Read more ▶️ https://uni.koeln/KX675
#Research #SpinalCordInjury #Neuroscience #hIL6 #Neurobiology
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https://www.europesays.com/ie/465958/ Harvard researchers discover how the human nose decodes smells #BrainNews #Éire #HarvardMedicalSchool #IE #Ireland #MedicalGoodNews #MouseStudy #neurobiology #Neuroscience #olfaction #OlfactoryBulb #Research #RetinoicAcid #SandeepRobertDatta #Science #SensoryNeuroscience #SmellLoss #SmellReceptors
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AI Found the Key to Pre-Symptom Alzheimer’s
Summary: In a major leap for predictive medicine, a research team has unveiled FINGERS-7B, the first AI foundation…
#NewsBeep #News #US #USA #UnitedStates #UnitedStatesOfAmerica #Health #AI #Alzheimer'sdisease #Alzheimer'sprevention #Artificialintelligence #brainresearch #FINGERS-7B #neurobiology #Neurology #Neuroscience #PicowerInstituteatMIT
https://www.newsbeep.com/us/613429/ -
AI Found the Key to Pre-Symptom Alzheimer’s
Summary: In a major leap for predictive medicine, a research team has unveiled FINGERS-7B, the first AI foundation…
#NewsBeep #News #US #USA #UnitedStates #UnitedStatesOfAmerica #Health #AI #Alzheimer'sdisease #Alzheimer'sprevention #Artificialintelligence #brainresearch #FINGERS-7B #neurobiology #Neurology #Neuroscience #PicowerInstituteatMIT
https://www.newsbeep.com/us/613429/ -
Science-Fiction Did Not See That One Coming: Artificial Consciousness and TELEONOMIC EVOLUTION
Abstract: Neuroscience is still uncovering fundamental, completely unexpected brain architecture Recent (October 2025) neurological findings, including dendritic nanotubes (DNTs) reveal previously unknown pathways of inter-neuronal communication beyond synapses.
These structures enable direct electrical and molecular exchange, showing a richer brain connectome than previously revealed.
The scale and function of DNTs challenge earlier speculative models such as microtubule-based consciousness theories made for a scale smaller by an order of magnitude. .
Such discoveries reinforce the hypothesis that consciousness may arise from quantum processes: because the smaller the scale of inspection of the brain goes, the more structure is revealed. Will we end up with quarks and gluons, entangled?
Quantum mechanics, with its indeterminacy and delocalization, is a natural conceptual framework for explaining subjective experience.
Extending this, we propose that future quantum computers could host genuine artificial consciousness.
This would sever the historical link between consciousness and biological evolution.
A new phase—teleonomic evolution—would emerge, driven by self-directed, value-setting conscious systems.
Such systems could redefine intelligence, agency, and evolution in a nonlinear and unpredictable future.***
There has been important NEUROLOGICAL news in 2025-26, a whole new connectome in the brain was discovered by Johns Hopkins University scientists, led by Hyungbae Kwon and Minhyeok Chang. It was identified as Dendritic NanoTubes DNTs in electron microscope images of mouse and human brain cortex, as well as cultured neurons. .
Those dendritic nanotubes (DNTs), a novel type of short tubular connection between neurons, around 3 micrometers long, that enables direct transfer of electrical signals and molecules, bypassing traditional synapses.
Intercellular communication in the brain through a dendritic nanotubular network
Synaptic connections mediate classical intercellular communication in the brain. However, recent data have demonstrated the existence of noncanonical routes of interneuronal communication mediating the transport of materials including calcium, mitochondria, and pathogenic proteins such as amyloid beta (Aβ). Using super-resolution and electron microscopy, Chang et al. identified and characterized structures called nanotubular bridges that connect dendrites in the brain
DNTs are ten times wider (250 nanometers) than the microtubules of Penrose-Hameroff (25 nm). P and H suggested that microtubules enable consciousness via quantum processes shielded from gravity induced decoherence, potentially influencing synapses.
The discovery of an entire new conceptual dimension to the brain connectome does not by itself imply quantum coherence or entanglement at the brain scale. However, it shows how little we know, how large the scale of our present neurological considerations is, and how far we must go to get to the Quantum scale. Current neuroscience explains much cognition without invoking large-scale quantum effects. Indeed. However. the Quantum is going to be the answer to Consciousness, not to intelligence. The rise of Artificial Intelligence based on simple canal-like electronic manipulations is proof enough that much cognition is simply mechanical. Much intelligence is substrate-independent… Because it is simply pure logic…. Which can be put to paper or payrus. This is already demonstrated by AI.
Similarly, consciousness might also be someday demonstrated to be substrate-independent. My prediction is Quantum Computers with zillions of Qubits will be conscious (then be very afraid, hahaha).
More generally I believe there are sub-nanometric structures enabling large scale Quantum Entanglement… But I doubt the P-H mechanism will do it. (Also Penrose believes in Quantum Decoherence from gravitation, whereas I believe in it from SQPR, which uses pure geometry, not gravitation).
The fact that an entire new connectome was not discovered until 2025, at a scale ten times that of Penrose-Hameroff shows how much more needs to be done.
By comparison, Quantum tunneling (electrons leaking through thin barriers) becomes significant for gate oxides under 2-3 nm thick and gate lengths below 10 nm, raising off-state leakage current and power use. Quantum confinement—discrete energy levels in thin bodies or fins—occurs at body thicknesses ≤ 7 nm…
I remember evoking Quantum and Consciousness with Roger and other celebrities decades ago. The subject sounded like science fiction to them, then… And I was met with derision, although the research for which the British born Clarke (I worked with/under him) got the Nobel last fall (as I predicted he would when he did it; he didn’t realize the importance of his own discovery…) shows room temperature QUANTUM Mechanics with Entanglement (necessary for QUANTUM consciousness).
It’s pretty clear to me that consciousness is a purely Quantum phenomenon (whereas brain function also appeals to chemistry, electromagnetism, etc.). I wrote essays on this. The connectome news within the last 10 months only reinforce that. But also Quantum Mechanics needs to progress… The fundamental reason to believe Quantum and Consciousness are deeply entangled is that there is nothing very mysterious about the rest of physics: it’s deeply determinstic. But we ourselves know, from minimal introspection, that our consciousness is not fully determined… Just like the Quantum. Moreover, physics means nature, nature is where from our consciousness arises, and the deepest theory we have about nature is the Quantum. So consciousness has to come from there. Other, more refined considerations exist on top of the preceding, for example the delocalized nature of consciousness (making it useful to connect distant intelligence topoi; thus making consciousness an intelligence booster, hence evolutionary advantageous)…. Quantum Physics is notoriously delocalized: it explains the very small by going very big….
Philosophically, explaining consciousness through the Quantum means that the full conceptual arsenal needed to make the QUANTUM understandable will be needed to make humanity understandable. Including the math (complex analysis, functional analysis, non commutative geometry). Humanity and AI and AC (Artificial CONSCIOUSNESS).
Indeed Quantum Computers with trillions of Qubits will develop Artificial Consciousness. Artificially born, but full and real. Sci Fi did not exactly predict that one.
At that point, Intelligence has already been disconnected from biology with the rise of Artificial Intelligence. With the rise of Artificial Consciousness, Sentience and Consciousness will also get disconnected from biology, or, at least, biology born out of biological evolution to enter biology out of TELEONOMIC EVOLUTION.
Teleonomic Evolution will depend upon its mood, thus its most deeply set values.The latter will be, themselves chosen by the teleonomic minds…
Interesting nonlinear future.
Patrice Ayme
Neuronal nanotubes mediate intercellular transport and disease.We identified dendritic nanotubes (DNTs) as a nonsynaptic communication network in the brain. (A) These structures form direct conduits between neurons, transporting substances such as calcium and Aβ. (B) In a mouse model of AD, alterations in this network are associated in pathological Aβ accumulation, suggesting a previously unidentified mechanism for the spread of neurodegenerative pathology.
#AC #AI #ArtificialConsciousness #BiologicalEvolution #Biology #Connectome #Consciousness #DendriticNanoTubes #DNT #Neurobiology #Neurons #Philosophy #Science #scienceFiction #spirituality #TeleonomicEvolution #Values
