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Tero Toivanen

AK's Rambling Thoughts: Nerve Cells and Glial Cells: Redefining the Foundation of Intel... - 0 views

artksthoughts.blogspot.com/...nd-glial-cells-redefining.html

brain Glial Cells neuron action potential axon synapse network microglia macroglia astrocytes oligodendrocytes ependymal cells radial glia

shared by Tero Toivanen on 25 Jun 09 - Cached
  • Glia are generally divided into two broad classes, microglia and macroglia. Microglia are part of the immune system, specialized macrophages, and probably don't participate in information handling. Macroglia are present in both the peripheral and central nervous systems, in different types.
  • Traditionally, there were four types of glia in the CNS: astrocytes, oligodendrocytes, ependymal cells, and radial glia. Of these, the one type that's most important to the developing revolution in our ideas are those cells called astrocytes.2 It turns out that there are at least two types of cell (at least) subsumed under this name.24, 25, 31, 32 One, which retains the name of astrocyte, takes up neurotransmitters released by neurons (and glial cells), aids in osmoregulation,10 controls circulation in the brain,1, 31 and generally appears to provide support for the neurons and other types of glia.
  • Although both NG2-glia and astrocytes extend processes to nodes of Ranvier in white matter ([refs]) and synapses in grey matter, their geometric relationship to these neuronal elements is different. Thus, although astrocytes and NG2-glia bear a superficial resemblance, they are distinguished by their different process arborizations. This will reflect fundamental differences in the way these two glial cell populations interact with other elements in the neural network.
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  • Both types of glia are closely integrated with the nervous system, receiving information from action potentials via synapses22 (which, only a few years ago were thought to be limited to neurons), and returning control of neuron activity through release of neurotransmitters and other modulators. Both, then, demonstrate the potential for considerable intelligent activity, contributing to the overall intelligence of the brain.
  • Astrocytes probably (IMO) are limited, or mostly so, to maintaining the supplies of energy and necessary metabolites. They receive action potentials,3, 6 which allows them to closely and quickly monitor general activity and increase circulation in response, even before the neurons and NG2-glia have reduced their supply of ATP.21 They appear to be linked in a network among themselves,2, 5 allowing them to communicate their needs without interfering with the higher-level calculations of the brain.
  • NG2-glia appear to have several functions, but one of the most exciting things about them is that they seem to be able to fire action potentials.33 Their cell membranes, like those of the dendrites of neurons, have all the necessary channels and receptors to perform real-time electrical calculations in the same way as neural dendrites. They have also demonstrated the ability to learn through long term potentiation.
  • Dividing NG2-glia also retain the ability to fire action potentials, as well as receiving synaptic inputs from neurons.23 Presumably, they continue to perform their full function, including retaining any elements of long term potentiation or depression contained in their synapses.
  • Oligodendrocytes are responsible for the insulation of the axons, wrapping around approximately 1 mm of each of up to 50 axons within their reach, and forming the myelin sheath.
  • Although the precise type of neuron formed by maturing cells hasn't been determined, the very fact that cells of this type can change into neurons is very important. We actually don't know whether the cells that do this maturation are the same as those that perform neuron-like activities, there appear to be two separate types of NG2-glia, spiking and non-spiking.26 It may very well be that the "spiking" type have actually differentiated, while the "non-spiking" type may be doing the maturing. Of course, very few differentiated cell types remain capable of division, as even the "spiking" type do.
  • What's important about both dendrites and NG2-glia isn't so much their ability to propagate action potentials, as that their entire cell membranes are capable of "intelligent" manipulation of the voltage across it.
  • While there are many ion channels involved in controlling the voltage across the cell membrane, the only type we really need to worry about for action potentials is voltage-gated sodium channels. These are channels that sometimes allow sodium ions to pass through the cell membrane, which they will do because the concentration of sodium ions outside the cell is very much higher than inside. When and how much they open depends, among other things, on the voltage across the membrane.
  • A normal neuron will have a voltage of around -60 to -80mV (millivolts), in a direction that tends to push the sodium ions (which are positive) into the cell (the same direction as the concentration is pushing). When the voltage falls to around -55mV, the primary type of gate will open for a millisecond or so, after which it will close and rest for several milliseconds. It won't be able to open again until the voltage is somewhere between -55 and around -10mV. Meanwhile, the sodium current has caused the voltage to swing past zero to around +20mV.
  • When one part of the cell membrane is "depolarized" in this fashion, the voltage near it is also depressed. Thus, if the voltage is at zero at one point, it might be at -20mV 10 microns (μm) away, and -40mV 20μm away, and -60mV 30μm, and so on. Notice that somewhere between 20μm and 30μm, it has passed the threshold for the ion channels, which means that they are open, allowing a current that drives the voltage further down. This will produce a wave of voltage drop along the membrane, which is what the action potential is.
  • After the action potential has passed, and the gates have closed (see above), the voltage is recovered by diffusion of ions towards and away from the membrane, the opening of other gates (primarily potassium), and a set of pumps that push the ions back to their resting state. These pumps are mostly powered by the sodium gradient, except for the sodium/potassium pump that maintains it, which is powered by ATP.
  • the vast majority of calculation that goes into human intelligence takes place at the level of the network of dendrites and NG2-glia, with the whole system of axons, dendrites, and action potentials only carrying a tiny subset of the total information over long distances. This is especially important considering that the human brain has a much higher proportion of glial matter than our relatives.
  • This, in turn, suggests that our overall approach to understanding the brain has been far too axon centric, there needs to be a shift to a more membrane-centric approach to understanding how the brain creates intelligence.
  • Tero Toivanen on 25 Jun 09
     
    Our traditional idea of how the brain works is based on the neuron: it fires action potentials, which travel along the axon and, when the reach the synapses, the receiving neuron performs a calculation that results in the decision when (or whether) to fire its own action potential. Thus, the brain, from a thinking point of view, is viewed as a network of neurons each performing its own calculation. This view, which I'm going to call the axon-centric view, is simplistic in many ways, and two recent papers add to it, pointing up the ways in which the glial cells of the brain participate in ongoing calculation as well as performing their more traditional support functions.
Tero Toivanen

Autism Blog - Autism: Is it all about bigger brains? « Left Brain/Right Brain - 0 views

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autism brain research cell division Glial Cells minicolumns

shared by Tero Toivanen on 26 Dec 09 - Cached
  • in light of the increased cranial volumn and minicolumnar density in autism, more recent studies have begun targeting certain proteins and steroids called Growth Factors, which are in part intimately involved in neocortical expansion.
  • Basic Fibroblast Growth Factor (bFGF or FGF2) has particularly important implications in autism given its involvement in prolonging the period of cell division of the number of undifferentiated radial glial cells (cortical stem cells) which determine the total number of eventual minicolumns: the longer these radial glial divide, the greater the number of minicolumns, like that seen in autism.
  • It’s fascinating to think that while autism can undoubtedly provide for its share of handicap, these foundational elements may be “abnormal” only in the sense that they’re extremes of those things which make us most human.
  • Tero Toivanen on 26 Dec 09
     
    Basic Fibroblast Growth Factor (bFGF or FGF2) has particularly important implications in autism given its involvement in prolonging the period of cell division of the number of undifferentiated radial glial cells (cortical stem cells) which determine the total number of eventual minicolumns: the longer these radial glial divide, the greater the number of minicolumns, like that seen in autism.
Tero Toivanen

Cord blood cell transplantation provides improvement for severely brain-injured child - 0 views

www.physorg.com/...-transplantation-severely.html

cell blood cord brain brain injury improvement research science

shared by Tero Toivanen on 22 Dec 10 - No Cached
  • Tero Toivanen on 22 Dec 10
     
    In three monthly injections, researchers transplanted neurally-committed, autologous cord blood derived cells tagged with iron oxide nanoparticles (SPIO) into the lateral cerebral ventricle of a 16-month old child with severe global hypoxic ischemic brain injury. The study is published in the current issue of Cell Medicine
Tero Toivanen

Alzheimer's discovery could lead to long-sought preventive treatment - 1 views

www.sciencedaily.com/...100108090951.htm

brain Alzheimer's discovery research preventive cells amyloid-beta

shared by Tero Toivanen on 08 Jan 10 - Cached
  • Tero Toivanen on 08 Jan 10
     
    The UCF team found that over time, though there are no outward signs of damage, exposure to moderate amyloid-beta concentrations somehow prevents electrical signals from traveling normally through the cells. Because the effect is seen in otherwise healthy cells, Hickman believes the team may have uncovered a critical process in the progression of Alzheimer's that could occur before a person shows any known signs of brain impairment.
Tero Toivanen

Scientists discover how brain cells age | KurzweilAI - 2 views

www.kurzweilai.net/s-discover-how-brain-cells-age

brain cells age research neuroscience neurons

shared by Tero Toivanen on 13 Sep 12 - No Cached
  • Tero Toivanen on 13 Sep 12
     
    "Now scientists at Newcastle University, led by Professor Thomas von Zglinicki, have shown that neurons in fact follow the same pathway as senescing fibroblasts, the cells that divide in the skin to repair wounds."
Tero Toivanen

Scientists capture the first image of memories being made - 0 views

www.eurekalert.org/...mu-sct061809.php

brain memory protein translation long-term memory proteins synapse synaptic connection learning synaptic plasticity post-synaptic cell neurons

shared by Tero Toivanen on 21 Jun 09 - Cached
  • A new study by researchers at the Montreal Neurological Institute and Hospital (The Neuro), McGill University and University of California, Los Angeles has captured an image for the first time of a mechanism, specifically protein translation, which underlies long-term memory formation. The finding provides the first visual evidence that when a new memory is formed new proteins are made locally at the synapse - the connection between nerve cells - increasing the strength of the synaptic connection and reinforcing the memory. The study published in Science, is important for understanding how memory traces are created and the ability to monitor it in real time will allow a detailed understanding of how memories are formed.
  • research has focused on synapses which are the main site of exchange and storage in the brain.
  • They form a vast but also constantly fluctuating network of connections whose ability to change and adapt, called synaptic plasticity, may be the fundamental basis of learning and memory.
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  • Using a translational reporter, a fluorescent protein that can be easily detected and tracked, we directly visualized the increased local translation, or protein synthesis, during memory formation.
  • Importantly, this translation was synapse-specific and it required activation of the post-synaptic cell, showing that this step required cooperation between the pre and post-synaptic compartments, the parts of the two neurons that meet at the synapse.
  • This study provides evidence that a mechanism that mediates this gene expression during neuronal plasticity involves regulated translation of localized mRNA at stimulated synapses.
  • Tero Toivanen on 21 Jun 09
     
    A new study by researchers at the Montreal Neurological Institute and Hospital (The Neuro), McGill University and University of California, Los Angeles has captured an image for the first time of a mechanism, specifically protein translation, which underlies long-term memory formation.
Tero Toivanen

NIMH · Our brains are made of the same stuff, despite DNA differences - 0 views

www.nimh.nih.gov/...-despite-dna-differences.shtml

nimh brains dna differences gene prefrontal cortex schizophrenia autism research study genetic variation neuroscience neurons

shared by Tero Toivanen on 30 Oct 11 - No Cached
  • “Having at our fingertips detailed information about when and where specific gene products are expressed in the brain brings new hope for understanding how this process can go awry in schizophrenia, autism and other brain disorders,” said NIMH Director Thomas R. Insel, M.D.
  • Among key findings in the prefrontal cortex:Individual genetic variations are profoundly linked to expression patterns. The most similarity across individuals is detected early in development and again as we approach the end of life.Different types of related genes are expressed during prenatal development, infancy, and childhood, so that each of these stages shows a relatively distinct transcriptional identity. Three-fourths of genes reverse their direction of expression after birth, with most switching from on to off.Expression of genes involved in cell division declines prenatally and in infancy, while expression of genes important for making synapses, or connections between brain cells, increases. In contrast, genes required for neuronal projections decline after birth – likely as unused connections are pruned.By the time we reach our 50s, overall gene expression begins to increase, mirroring the sharp reversal of fetal expression changes that occur in infancy.Genetic variation in the genome as a whole showed no effect on variation in the transcriptome as a whole, despite how genetically distant individuals might be. Hence, human cortexes have a consistent molecular architecture, despite our diversity.
  • Among key findings:Over 90 percent of the genes expressed in the brain are differentially regulated across brain regions and/or over developmental time periods. There are also widespread differences across region and time periods in the combination of a gene’s exons that are expressed.Timing and location are far more influential in regulating gene expression than gender, ethnicity or individual variation.Among 29 modules of co-expressed genes identified, each had distinct expression patterns and represented different biological processes. Genetic variation in some of the most well-connected genes in these modules, called hub genes, has previously been linked to mental disorders, including schizophrenia and depression.Telltale similarities in expression profiles with genes previously implicated in schizophrenia and autism are providing leads to discovery of other genes potentially involved in those disorders.Sex differences in the risk for certain mental disorders may be traceable to transcriptional mechanisms. More than three-fourths of 159 genes expressed differentially between the sexes were male-biased, most prenatally. Some genes found to have such sex-biased expression had previously been associated with disorders that affect males more than females, such as schizophrenia, Williams syndrome, and autism.
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  • Our brains are all made of the same stuff. Despite individual and ethnic genetic diversity, our prefrontal cortex shows a consistent molecular architecture.
  • Males show more sex-biased gene expression. More genes differentially expressed (DEX) between the sexes were found in males than females, especially prenatally. Some genes found to have such sex-biased expression had previously been associated with disorders that affect males more than females, such as schizophrenia, Williams syndrome, and autism.
  • Tero Toivanen on 30 Oct 11
     
    Our brains are all made of the same stuff. Despite individual and ethnic genetic diversity, our prefrontal cortex shows a consistent molecular architecture. 
Tero Toivanen

'Noisiest' neurons persist in the adult brain - 0 views

www.physorg.com/news182609011.html

neurons neuroscience brain survival epilepsy hyperactive molecular signals neuronal activity

shared by Tero Toivanen on 18 Jan 10 - Cached
  • In addition, the observation that the "noisiest" neurons have a survival advantage helps explain the prevalence of epilepsy, in which some neurons become hyperactive and fire in an uncontrollable fashion.
  • during childhood, when many neurons are still being added to the brain, it is likely that neurons that become pathologically hyperactive will be preferentially selected for survival, and these abnormal neurons will be the trigger for epilepsy,
  • Investigating the molecular signals launched by neuronal activity will potentially lead to new drugs that bolster the survival of new neurons. These drugs could be used to increase the efficacy of treatments that depend on grafting stem cell-derived neurons into the adult brain to treat neurological diseases such as Parkinson's and Alzheimer's.
  • Tero Toivanen on 18 Jan 10
     
    'Noisiest' neurons persist in the adult brain
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