R Douglas Fields
https://www.researchgate.net/publication/266624474_Myelination_of_the_Nervous_System_Mechanisms_and_Functions
Myelination of the Nervous System: Mechanisms and Functions
DOI: 10.1146/annurev-cellbio-100913-013101 · Source: PubMed
Myelination of the Nervous System: Mechanisms and Functions (PDF Download Available). Available from:
https://www.researchgate.net/publication/266624474_Myelination_of_the_Nervous_System_Mechanisms_and_Functions [accessed Feb 14 2018].
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(Vallitsevan teorian kehittämisen pioneerit ja suuret nimet merkitty punaisella ja linkitetty, kriteerinä erityisesti, että R. D. Fields on kertonut tutkimuksista aiheen perusteoksissaan, HM, suomalaiset henkilöt ja tutkimukset merkitty sinisellä.)
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She’s 17 years old and already helping patients. Meet the winner of one of the country’s most prestigious science fairs.
Indrani Das has been fascinated with brain injuries since her freshman year of high school, when she learned that their effects can be devastating and irreversible.
Later, her fascination evolved into a full-fledged research project. Das, now 17 and a senior at the Academy for Medical Science Technology in Hackensack, N.J., ex-plored how brain damage occurs, examining a process called astrogliosis, which can lead to the excess production of a toxin that can damage neurons. If she and other researchers could better understand how brain damage occurs, perhaps they could figure out how to slow or reverse the process.
“My work centers on repairing the behavior of supporting cells to prevent neuron in-jury and death,” Das said. “It was really that shock of what it can do to a person that pushed me to work” on research involving brain injuries.
Das’s project, which explores the role of brain cells called astrocytes in the death of neurons, was awarded the top prize and $250,000 at the Regeneron Science Talent Search.
Das bested thousands of high school scientists from across the country. The talent search selected 40 finalists, who traveled last week to D.C., where a selection com-mittee grilled them on their work and put them through the wringer, testing their grasp of scientific concepts and their ability to solve problems.
Four of the finalists were from the Washington area: Prathik Naidu of Thomas Jef-ferson High School for Science and Technology in Fairfax County; David Rekhtman of Walt Whitman High School in Bethesda; and Sambuddha Chattopadhyay and Rohan Dalvi, both of Montgomery Blair High School in Silver Spring.
Naidu placed seventh, taking home $70,000 for his project, which created 3-D models of the genetics of cancer cells, using a computer program he built.
The Science Talent Search, previously sponsored by Intel, is one of the best-known and among the most competitive science fairs for young researchers. This year, the talent search gave out $1.8 million to 40 finalists, much of which will go to cover college tuition for the budding researchers.
[These teens are working to cure cancer and solve the mysteries of the universe]
Maya Ajmera, president and chief executive of the Society for Science and the Pub-lic, said the finalists are often well-rounded and driven by their desire to make the world a better place, an altruism that is reflected in extracurricular activities.
Das, who hails from Orendell, N.J., recently became a certified emergency medical technician and is already working with patients, helping to transport them to hospitals. While she is deeply fascinated by research, she also hopes to become a practicing physician so she can work with patients.
“I would say my happiest time is when I’m with my patients,” Das said. “I love connecting with people and understanding how I can help them. It keeps me human.”
She plans to use the prize money to help pay for college and medical school.
Nonsynaptic junctions on myelinating glia promote preferential myelination of electrically active axons
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4439926/
Physiological Function of Microglia
Role of Myelin Plasticity in Oscillations and Synchrony of Neuronal Activity
https://science.howstuffworks.com/life/inside-the-mind/human-brain/remember-birth.htm
Can a person remember being born?
Think back to your earliest memory. Perhaps images of a birthday party or scenes from a family vacation come to mind. Now think about your age when that event oc-curred. Chances are that earliest recollection extends no further back than your third birthday. In fact, you can probably come up with only a handful of memories from be-tween the ages of 3 and 7, although family photo albums or other cues may trigger more.
Psychologists refer to this inability of most adults to remember events from early life, including their birth,as childhood amnesia.Sigmund Freud first coined the term infan- tile amnesia, now more broadly referred to as childhood amnesia,as early as 1899 to explain his adult patients' scarcity of childhood memories [source: Rapaport]. Freud proposed that people use it as a means of repressing traumatic, and often sexual, urgings during that time. To block those unconscious drives of the id, Freud claimed that humans create screen memories, or revised versions of events, to protect the conscious ego. "
Puutaheinää. Oikea selitys täällä:
CG: " More than a century later, researchers have yet to pin down a precise expla-nation for why childhood amnesia occurs. Only in the last 20 years have people in-vestigated children's,rather than adults',memory capabilities in search of the answer. This research has brought with it a new batch of questions about the nuances of young children's memory.
For a long time, the rationale behind childhood amnesia rested on the assumption that the memory-making parts of babies' brains were undeveloped. Then, around age 3, children's memory capabilities rapidly accelerate to adult levels. "
T.: Näinkin voi sanoa. Mutta kielen oppiminen nimenomaan luo myös ne aivojen ka-pasiteetit, joille ihmisen ajattelu perustuu. Tämän huomasi jo 1700-luvulla englanti-lainen psykiatri David Hartley alun perin fyysiä aivoja tutkimalla vastikään kehitetyllä mikroskoopilla.
CC: " However, psychologists have discovered that children as young as 3 months old and 6 months old can form long-term memories. "
T.: Yes. Suoria ehdollisia refleksejä. Niitä ei muisteta sellaisinaan, vaan muiden, kie-lellisten muistojen yhteydessä,joiden muodostumiseen ne vaikuttavat ollen alun perin näiden rakennuspalikkoina, jotka kootaan kielellisesti muistettaviksi muistoiksi.
https://science.howstuffworks.com/life/inside-the-mind/human-brain/remember-birth1.htm
... CC: " The difference comes in which memories stick around. For instance, it appears that babies are born with more intact implicit, or unconscious, memories. "
T.: Ehdottomia refleksejä EI pidä nimittää lainkaan "MUISTOIKSI" eikä tajunnaksi, koska ne eivät ole sitä. Suorat ehdolliset refleksit sellaisenaan eivät myöskään ole tajuntaa. Ne ovat sitä, millä esimerkiksi simpanssi käyttäytyy, ja mekin kävelemme ja juoksemme pystyssä ja pidämme myös polkupyörää ja moottoripyörää pystyssä ajaessamme. (Koska muuten tekoäly oppii ajamaan moottoripyörällä? Sitä ennen ei kannata puhua TIETOISESTA tekoälystä, sillä tuo tehtävä on HELPOMPI.)
CC: " At the same time the explicit, or episodic, memory that records specific events does not carry information over that three-year gap, explaining why people do not remember their births.
But why does this happen, and what changes take place in those first years? And if we can form memories as babies, why don't we retain them into adulthood?
On the next page, we'll take a closer look at a baby's brain to find out the answer.
Memory Encoding in Children
To form memories,humans must create synapses,or connections between brain cells (linkitys lähteen, T.), that encode sensory information from an event into our memory. From there, our brains organize that information into categories and link it to other similar data, which is called consolidation. In order for that memory to last, we must periodically retrieve these memories and retrace those initial synapses, reinforcing those connections.
Studies have largely refuted the long-held thinking that babies cannot encode infor-mation that forms the foundation of memories. For instance, in one experiment invol-ving 2- and 3-month-old infants, the babies' legs were attached by a ribbon to a mo-bile [source: Hayne]. By kicking their legs, the babies learned that the motion caused the mobile to move. Later, placed under the same mobile without the ribbon, the in-fants remembered to kick their legs. When the same experiment was performed with 6-month-olds, they picked up the kicking relationship much more quickly, indicating that their encoding ability must accelerate gradually with time, instead of in one significant burst around 3 years old.
This memory encoding could relate to a baby's development of the prefrontal cortex at the forehead. This area, which is active during the encoding and retrieval of expli-cit memories, is not fully functional at birth [source: Newcombe et al]. However, by 24 months, the number of synapses in the prefrontal cortex has reached adult levels [source: Bauer].
Also, the size of the hippocampus at the base of the brain steadily grows until your second or third year [source: Bauer]. This is important because the hippocampus determines what sensory information to transfer into long-term storage.
https://science.howstuffworks.com/life/inside-the-mind/human-brain/remember-birth2.htm
"... But what about implicit memory? Housed in the cerebellum, implicit memory is essential for newborns, allowing them to associate feelings of warmth and safety with the sound of their mother's voice and instinctively knowing how to feed. Confirming this early presence,studies have revealed few developmental changes in implicit me- mory as we age [source: Newcombe et al]. Even in many adult amnesia cases, impli-cit skills such as riding a bicycle or playing a piano often survive the brain trauma.
Now we know that babies have a strong implicit memory and can encode explicit ones as well, which indicates that childhood amnesia may stem from faulty explicit memory retrieval. Unless we're thinking specifically about a past event,it takes some sort of cue to prompt an explicit memory in all age groups [source: Bauer]. Up next, find out what those cues are. "
T.: Kyse ei ole vain "palautusvirheestä",vaan siitä, että ihmiselle ominainen kielellis-rakenteinen tajunta on vasta muodostumassa ympäristöstä riippumattomalla tavalla ajatuksellisesti mieleenpalautettavissa olevine muistoineen.
CC: " Language and Sense of Self in Memory-Making
Our earliest memories may remain blocked from our consciousness because we had no language skills at that time.A 2004 study traced the verbal development in 27- and 39-month old boys and girls as a measure of how well they could recall a past event. The researchers found that if the children didn't know the words to describe the event when it happened, they couldn't describe it later after learning the appropriate words [source: Simcock and Hayne].
Verbalizing our personal memories of events contributes to our autobiographical memories. These types of memories help to define our sense of self and relationship to people around us. Closely linked to this is the ability to recognize yourself. Some researchers have proposed that children do not develop self-recognition skills and a personal identity until 16 or 24 months [source: Fivush and Nelson].
In addition, we develop knowledge of our personal past when we begin to organize memories into a context.
Many preschool-age children can explain the different parts of an event in sequential order, such as what happened when they went to a circus. But it isn't until their fifth year that they can understand the ideas of time and the past and are able to place that trip to the circus on a mental time line [source: Fivush and Nelson].
Parents play a pivotal role in developing children's autobiographical memory as well. Research has shown that the way parents verbally recall memories with their small children correlates to those children's narrative style for retelling memories later in life. In other words, children whose parents tell them about past events, such as birth- day parties or trips to the zoo, in detail will be more likely to vividly describe their own memories [source: Urshwa]. Interestingly, autobiographical memory also has a cultu-ral component, with Westerners' personal memories focusing more on themselves and Easterners remembering themselves more in group contexts [source: Urshwa].
More detailed explanations exist regarding childhood amnesia. But brain structure, language and sense of self are its foundation. To learn more about amnesia and memory, don't forget to read the links below. ...
Primal Healing
Flying in the face of childhood amnesia research,some people claim to recall prever- bal memories and even recollections from the womb. One form of psychoanalysis, called primal healing, focuses on traumatic early memories similar to Sigmund Freud's theory of repressed and screen memories.Primal therapy links people's pre- sent pain with the pain of birth,taking patients back to the memory of their own birth in a process referred to as rebirthing. However,in spite of anecdotal evidence, no scien- tific study has verified the authenticity of these rebirthing experiences [source:Eisner]. "
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Dr. Douglas Fields: "Exploring New Frontiers in Neuroscience" | Talks at Google
Nonsynaptic junctions on myelinating glia promote preferential myelination of electrically active axons
Abstract
The myelin sheath on vertebrate axons is critical for neural impulse transmission, but whether electrically active axons are preferentially myelinated by glial cells, and if so, whether axo-glial synapses are involved, are long-standing questions of significance to nervous system development, plasticity and disease. Here we show using an in vitro system that oligodendrocytes preferentially myelinate electrically active axons, but synapses from axons onto myelin-forming oligodendroglial cells are not required. Instead, vesicular release at nonsynaptic axo-glial junctions induces myelination. Axons releasing neurotransmitter from vesicles that accumulate in axon varicosities induces a local rise in cytoplasmic calcium in glial cell processes at these nonsynap-tic functional junctions, and this signalling stimulates local translation of myelin basic protein to initiate myelination.
The surprising discovery of synapses formed on glial progenitors, oligodendrocyte progenitor cells (OPCs, also called NG2 cells) has remained enigmatic for over a decade1.These cells mature to form myelin insulation on axons2,3, and several func- tions for synapses on OPCs have been proposed4.A leading hypothesis is that axon-OPC synapses may stimulate myelination selectively on electrically active axons to increase the speed of impulse transmission through electrically active neural circuits 5,6. This would have significant effects on neural circuit function. Since myelination continues in many brain regions through early life, preferential myelination of electri-cally active axons could enable environmental factors to modify neural circuit development according to functional experience7.
Synapses on OPCs could increase myelination in an activity-dependent manner in several ways,including promoting OPCs to differentiate into mature oligodendrocytes or by increasing OPC survival or proliferation. However,signals from axons must also regulate initiation of myelin wrapping even after OPCs have matured,because mature oligodendrocytes can be associated with axons early in development but not form myelin until much later in prenatal or adult life 8. It has been shown that vesicular release of glutamate from axons stimulates local translation of myelin basic protein (MBP) and stimulates myelin induction9.This signalling could be mediated by synap- tic transmission or by spillover of neurotransmitter from axo-glial synapses activating extrasynaptic glutamate receptors on OPC processes10,11.
Alternatively to synaptic transmission, other forms of axo-glial communication could signal electrical activity in axons to OPCs. Nonsynaptic release of neurotransmitter operates by both vesicular and non-vesicular release mechanisms. Neurotransmit-ters can be released in the absence of morphological synaptic contacts to activate neurotransmitter receptors on other cells (volume conduction)12. In contrast to synap-tic communication, which is a specialization for rapid (millisecond) and highly point-to-point localized signalling between axons and dendrites,volume transmission could be particularly well suited for communication between axons and myelinating glia13. Vesicle fusion is seen at axonal swellings (varicosities) that lack identifying features of a synapse. Notably missing are the close apposition of pre- and post-synaptic membranes, submembrane thickening caused by cytoskeletal proteins that organize neurotransmitter receptors and intracellular signalling molecules in the postsynaptic apparatus and the focused accumulation of synaptic vesicles docked at the presy-naptic membrane. Neurotransmitter signalling at axonal varicosities along nerve fib-res is characteristic of autonomic transmission in the enteric nervous system14 and cholinergic transmission in neocortex15, but most neurons have similar axon varico-sities. In addition to nonsynaptic vesicular release, neurotransmitters also can be released along axons through membrane channels16.
Another important question is if given a choice,will oligodendroglial cells preferential- ly myelinate electrically active axons? In addition, oligodendrocytes are multipolar cells but it is unknown how different branches of the same oligodencrocyte are instructed by axons to act autonomously and selectively synthesize myelin in those processes that are in contact with active axons. In the present experiments, calcium imaging, electron microscopy and electrophysiology were used to determine the involvement of axon-glia communication in myelination of electrically active axons in vitro. The results indicate a strong preference for oligodendrocytes to myelinate elect-rically active axons via a mechanism dependent on nonsynaptic vesicular release of glutamate but independent of synapses on OPCs.
Results
Preferential myelination of electrically active axons
The hypothesis that axons that are electrically active would be preferentially myelina-ted was tested by co-culturing OPCs with neurons that could release synaptic vesicles together with other neurons in which vesicular release was blocked. Dorsal root ganglion (DRG) neurons were used in these studies because they have several advantages. DRG neurons have no dendrites and thus they are ideal for studying oligodendrocyte interactions with axons. The long central axons of DRG neurons are myelinated by oligodendrocytes, and DRG neurons do not form synapses on them-selves (in vivo or in culture)17,18. DRG neurons do not fire action potentials sponta-neously, and they fire a single action potential in response to a brief electrical stimu-lus; thus, the firing frequency and pattern can be regulated precisely by electrical sti-mulation of neurons in cell culture.In these experiments,half of the neurons were trea- ted with the clostridial neurotoxin, botulinum A (BoNT/A) together with a blue dye to identify these axons.BoNT/A is a potent and highly selective enzyme that cleaves sy- naptosome-associated protein-25 (SNAP-25), the t-SNARE (Target membrane-asso-ciated soluble N-ethylmaleimide-sensitive factor attachment protein receptor) neces-sary for neurotransmitter release from synaptic vesicles. The other half of the neurons were untreated,providing OPCs a choice as to which axons to myelinate once under- going differentiation.After washing out the toxin,which continues to inhibit neurotrans- mitter release for at least 4 weeks19, OPCs were added to neuronal cultures contai-ning normal and BoNT/A-treated neurons to determine whether myelin formed prefe-rentially on axons that release synaptic vesicles in response to electrical stimulation (Fig. 1a,b; Supplementary Fig. 1b–d). Compact myelin was identified by immunocyto-chemistry for MBP 3 weeks after culturing OPCs on DRG axons.
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