KESKUSTELU

8. Section: BRAIN SCIENCE

Although scientists have long regarded the brain's white matter as passive infrastructure, new work shows that it actively affects learning and mental illness.

KEY CONCEPTS

• White matter, long thought to be passive tissue, actively affects how the brain learns and dysfunctions.

• Although gray matter (composed of neurons) does the brain's thinking and calculating, white matter (composed of myelin-coated axons) controls the signals that neurons share, coordinating how well brain regions work together.

• A new type of magnetic resonance technology, called diffusion tensor imaging (DTI), has for the first time shown white matter in action, revealing its underappreciated role
.
• Myelin is only partially formed at birth and gradually develops in different regions throughout our 20s. The timing of growth and degree of completion can affect learning, self-control (and why teenagers may lack it), and mental illnesses such as schizophrenia, autism and even pathological lying.

--The Editors

Imagine if we could peek through the skull to see what makes one brain smarter than another. Or to discover whether hidden traits might be driving a person's schizophrenia or dyslexia. A new kind of imaging technique is helping scientists observe such evidence, and it is revealing a surprise: intelligence, and a variety of mental syndromes, may be influenced by tracts within the brain made exclusively of white matter.

Gray matter, the stuff between your ears your teachers chided you about, is where mental computation takes place and memories are stored. This cortex is the "topsoil" of the brain; it is composed of densely packed neuronal cell bodies--the decision-making parts of nerve cells, or neurons. Underneath it, however, is a bedrock of "white matter" that fills nearly half of the human brain--a far larger percentage than found in the brains of other animals. White matter is composed of millions of communications cables, each one containing a long, individual wire, or axon, coated with a white, fatty substance called myelin. Like the trunk lines that connect telephones in different parts of a country, this white cabling connects neurons in one region of the brain with those in other regions.

For decades neuroscientists exhibited little interest in white matter. They considered the myelin to be mere insulation and the cables inside it little more than passive passageways. Theories about learning, memory and psychiatric disorders centered on molecular action inside the neurons and at the famous synapses the tiny contact points between them. But scientists are now realizing that we have underestimated the importance of white matter in the proper transfer of information among brain regions. New studies show that the extent of white matter varies in people who have different mental experiences or who have certain dysfunctions. It also changes within one person's brain as he or she learns or practices .1 skill such as playing the piano. Even though the neurons in gray matter execute mental and physical activities, the functioning of white matter may be just as critical to how people master mental and social skills, as well as to why it is hard for old dogs to learn new tricks.

More with Mastery

The myelin that gives white matter its color has always posed mysteries. For more than a century scientists looked at neurons through their microscopes and saw long fibers, the axons, extending from a neuronal cell body to a neigh boring one, like an outstretched, elongated finger. Each axon was found to be coated with a thick crystalline gel. Anatomists surmised that the fatty covering must insulate axons like rubber sheathing along a copper wire. Strangely, however, many axons, especially the smaller filaments, were not coated at all. And even along insulated fibers, gaps in the insulation appeared every millimeter or so. The bare spots came to be known as nodes of Ranvier, after French anatomist Louis-Antoine Ranvier, who first described them.

Modern investigation has revealed that nerve impulses race down axons on the order of 100 times faster when they are coated with myelin and that myelin is laid on axons somewhat like electrical tape, wrapped up to 150 times between every node. The substance is manufactured in sheets by two types of glial cells. These cells are not neurons, but they are prevalent in the brain and nervous system [see "The Other Half of the Brain," by R. Douglas Fields; SCIENTIFIC AMERICAN, April 2004]. Anoctopus-shaped glial cell called an oligodendrocyte does the wrapping. Electrical signals, unable to leak out through the sheath, jump swiftly down the axon from node to node. In nerves outside the brain and spinal cord, a sausage-shaped glial cell called a Schwann cell forms myelin.

Without myelin, the signal leaks and dissipates. For maximum conduction velocity, the insulation thickness must he strictly proportional to the diameter of the fiber inside. The optimal ratio of bare axon diameter divided by the total fiber diameter (including the myelin) is 0.6. We have no idea how oligodendrocytes "know" whether 10 or 100 layers of insulation are required to create the proper thickness on axons of different diameters. But recently biologist Klaus-Armin Nave of the Max Planck Institute for Experimental Medicine in Göttingen, Germany, discovered that Schwann cells detect a protein called neuregulin that coats axons, and if the amount of this protein is augmented or inhibited, the Schwann cell will wrap more or fewer sheets of myelin around the axon. Interestingly, many people who suffer bipolar disorder or schizophrenia have a detect in the gene that regulates production of this protein.

The wrapping occurs at different ages. Myelin is prevalent only in a few brain regions at birth, expands in spurts and is not fully laid until age 25 or 30 in certain places. Myelination generally proceeds in a wave from the back "I the cerebral cortex (shirt collar) to its trout (forehead) as we grow into adulthood. The frontal lobes are the last places where myelination occurs. These regions are responsible for higher-level reasoning, planning and judgment--skills that only come with experience. Researchers have speculated that skimpy fore brain myelin is one reason that teenagers do not have adult decision-making abilities. Such observations suggest that myelin is important to intelligence.

Presumably the brain does not finish wrapping human axons until early adulthood because, throughout that time, axons continue to grow, gain new branches and trim others in response to experience. Once axons are myelinated, the changes they can undergo become more limited. Still, for a long time a question remained: Is myelin formation totally programmed, or do our life experiences alter the degree of wrapping and thus how well we learn? Does myelin actually build cognitive ability, or is cognition simply limited in regions where it has not yet formed?

Piano virtuoso Fredrik Ullén decided to find out. Ullén also happens to be an associate professor at the Stockholm Brain Institute in Sweden. In 2005 he and his colleagues used a new brain scanning technology called diffusion tensor imaging (DTI) to investigate the brains of professional pianists. DTI is done with the same kind of magnetic resonance imaging machines found in hospitals but involves a different type of magnetic field and different algorithms to create the many brain-image slices that are assembled into a three-dimensional picture. The slices display the vectors (mathematically defined as tensors) of water that diffuses in tissue. In gray matter the DTI signals are low because water diffuses symmetrically. But water diffuses asymmetrically along bundles of axons; this irregular pattern illuminates while mailer, exposing the major highways of information that flow among brain regions. The more tightly-packed and heavily coated with myelin the fibers are, the stronger the DTI signal.

Ullé found that in professional pianists, certain white matter regions are more highly developed than in nonmusicians. These regions connect parts of the cerebral cortex that are crucial to coordinated movement of the fingers with areas involving other cognitive processes that operate when making music.

He also found that the more hours a day a musician had practiced over time, the stronger the DTI signals were in these while matter tracts; the axons were more heavily myelinated or tightly packed. Of course, the axons could simply have expanded, requiring more myelin to maintain the optimal 0.6 ratio. Without performing an autopsy, the question remains open. The discovery is important, however, because it shows that when learning a complex skill, noticeable changes occur in white matter--a brain structure that contains no neuronal cell bodies or synapses, only axons and glia. Studies on animals, in which brains can be physically examined, show myelin can change in response to mental experience and a creature's developmental environment. Recently neurobiologist William T. Greenough of the University of Illinois at Urbana-Champaign confirmed that rats raised in "enriched" environments (with access to abundant toys and social interaction) had more myelinated fibers in the corpus callosum--the hefty bundle of axons that connects the brain's two hemispheres.

These results seem to jibe with DTI studies performed by neuroscientist Vincent J. Schmithorst of Cincinnati Children's Hospital, which compared white matter in children ages five to 18. A higher development of white matter structure, Schmithorst found, correlates directly with higher 1Q. Other reports reveal that children who suffer severe neglect have up to 17 percent less white matter in the corpus callosum.

Stimulating Change

Such findings strongly suggest that experience influences myelin formation and that the resulting myelin supports learning and improvement of skills. But to be fully convinced of that conclusion, investigators need a plausible explanation of how abundant myelin can enhance cognition, as well as some direct evidence that defects can impair mental abilities.
My lab has uncovered several ways in which an individual's experiences can influence myelin formation. In the brain, neurons fire electrical impulses down axons; by growing neurons from fetal mice in culture dishes equipped with platinum electrodes, we can impose patterns of impulses on them. We found that these impulses can regulate specific genes in neurons. One of the genes causes production of a sticks protein called L1-CAM that is crucial for pasting the first layer of membrane around an axon as myelin begins to form.

We also found that glia can "listen in" on impulses shooting through axons and that the traffic heard alters the degree of myelination; a type of glial cell called an astrocyte releases a chemical factor when it senses increased impulse traffic. This chemical code stimulates oligodendrocytes to form more myelin. Children who succumb to Alexander disease, a fatal childhood disorder causing mental retardation and abnormal myelin, have a mutation of an astrocyte gene.
Logic, too, helps to explain how white matter can influence cognitive ability. It might seem that, by analogy to the Internet, all information in the brain should be transmitted as quickly as possible. That would mean all axons should be equally myelinated. But for neurons, faster is not always better. Information must travel enormous distances between brain centers. Each center carries out its particular function and sends the output to another region for the next step of analysis. For complex learning, such as learning the piano, information must be shuttled back and forth among many regions; information flowing over different distances must arrive simultaneously at one place at a certain time. For such precision to occur, delays are necessary. If all axons transmitted information at the maximum rate, signals from distant neurons would always arrive later than signals from neighboring neurons. An impulse typically takes 30 milliseconds to travel from one cerebral hemisphere to the other through myelinated axons in the corpus callosum, compared with 150 to 300 milliseconds through unmyelinated axons. None of the corpus callosum's axons are myelinated at birth, and by adulthood 30 percent remain that way. The variation helps to coordinate transmission speeds.
Perhaps just as crucial are the nodes of Ranvier. In the past few years scientists have concluded that far from being mistakes, the nodes act as intricate, bioelectric repeaters--relay stations that generate, regulate and rapidly propagate electrical signals along an axon. By studying owls' excellent hearing, neurobiologists have shown that during myelination the oligodendrocytes insert more nodes than are optimal for fast signaling along certain axons to slow signals traveling along them.

Clearly, the speed of impulse transmission is a vital aspect of brain function. We know that memory and learning occur when certain neuronal circuits connect more strongly. It seems likely that myelin affects this strength, by adjusting conduction velocity so that volleys of electrical impulses arrive at the same neuron simultaneously from multiple axons. When this convergence occurs, the individual voltage blips pile up, increasing the strength of the signal, thus making a stronger connection among the neurons involved. Much more research must be done to explore this theory, but there is no doubt that myelin responds to the environment and participates in learning skills.

Learning and Mental Illness

With this new perspective, it is not hard to imagine how faulty transmission could lead to mental challenges. After decades of searching gray matter for the causes of mental disabilities, neuroscientists now have circumstantial evidence suggesting that white matter plays a role. Dyslexia, for example, results from disrupted timing of information transmission in circuits required for reading; brain imaging has revealed reduced white matter in these tracts, which could cause such disruption. The white matter abnormalities are thought to reflect both defects in myelination and developmental abnormalities in neurons affecting these white matter connections.

Tone deafness results from defects in higher-level processing in the cerebral cortex where sounds are analyzed; psychologist Kristi L. Hyde of McGill University has found that white matter is reduced in a specific fiber bundle in the right forebrain of tone-deaf individuals. Furthermore, recent research by Leslie K. Jacobsen of Yale University indicates that exposure to tobacco smoke during late fetal development or adolescence, when this bundle is undergoing myelination, disrupts the white matter. The structure, as seen by DTI, correlates directly with performance on auditory tests. Nicotine is known to affect receptors on oligodendrocytes that regulate the cells' development. Exposure to environmental factors during crucial periods of myelination can have lifelong consequences.

Schizophrenia is now understood to be a developmental disorder that involves abnormal connectivity. The evidence is multifold. Doctors have always wondered why schizophrenia typically develops during adolescence--but recall that this is the primary age when the forebrain is being myelinated. The neurons there have largely been established, but the myelin is changing, making it suspect. In addition, nearly 20 studies in recent years have concluded that white matter is abnormal (possessing fewer oligodendrocytes than it should) in several regions of the schizophrenic brain. And when gene chips--tiny diagnostic devices that can survey thousands of genes at a time--recently became available, researchers were startled to discover that many of the mutated genes linked to schizophrenia were involved in myelin formation. White matter abnormalities have also been found in people affected by ADHD, bipolar disorder, language disorders, autism, cognitive decline in aging and Alzheimer's disease and even in individuals afflicted with pathological lying.

Of course, underdeveloped or withered myelin could be a result of poor signaling among neurons, not necessarily a cause. After all, cognitive function does depend on neuronal communication across synapses in the cortex's gray matter, where most psychoactive drugs act. Yet optimal communication among brain regions, which is also fundamental to proper cognition, depends on the white matter bedrock connecting the regions. In 2007 Gabriel Corfas, a neurologist at Children's Hospital Boston, showed that experimental disruption of genes in oligodendrocytes--not in neurons--of mice causes striking behavioral changes that mimic schizophrenia. And the behavioral effects involve one of the same genes, neuregulin, found to be abnormal in biopsies of schizophrenic brains.
The chicken-and-egg question of whether changes in myelin alter neurons or whether changing neuronal patterns alter myelin will be settled the same way such dilemmas always are: with the acknowledgment that there is a close interdependence between the two mechanisms. Myelinating glia can respond to changes in axon diameter, but they also regulate that diameter. And they can determine whether or not a given axon survives. In multiple sclerosis, for example, axons and neurons can die after myelin is lost as a result of the disease.

Remodeling Old Age

Whatever the mechanism, as our brain matures from childhood to adulthood the precision of connections among regions improves. How well the connections are made may dictate how well we can learn certain skills at certain ages.
Indeed, Ullén's studies of accomplished pianists revealed an additional finding: white matter was more highly developed throughout the brains of individuals who had taken up the instrument at an earlier age. In people who learned after adolescence, white matter development was increased only in the forebrain--the region that was still undergoing myelination.

This finding suggests that the insulating of nerve fibers in part determines age limits for learning new skills--windows of opportunity, or critical periods, when certain learning can occur or at least can occur readily. Learn a foreign language after puberty, and you are destined to speak it with an accent; learn the language as a child, and you will speak it like a native. The difference occurs because the brain circuits that detect speech rewire according to the sounds we hear only as a child. We literally lose the connections that would allow us to hear sounds unique to foreign languages. In evolutionary terms, the brain has no reason to retain connections to detect sounds that it has never heard after years of childhood. Critical periods are also one of the main reasons adults do not recover as well from brain injuries as children do.

Specialists have identified specific protein molecules in myelin that stop axons from sprouting and forming new connections. Martin E. Schwab, a brain researcher at the University of Zurich, revealed the first of several myelin proteins that cause young sprouts from axons to wither instantly on contact. When this protein, which he named Nogo (now referred to as Nogo-A), is neutralized, animals with a spinal cord injury can repair their damaged connections and recover sensation and movement. Recently Stephen M. Strittmatter of Yale found that the critical period for wiring the brains of animals through experience could be reopened by blocking signals from Nogo. When the protein is disrupted in old mice, the critters can rewire connections for vision.
If myelination is largely finished in a person's 20s, however, does that contradict recent claims that the brain remains plastic throughout middle and old age? For example, studies show that mental exercise into a person's 60s, 70s and 80s helps to delay the onset of Alzheimer's. And how does a person's wisdom increase over the decades? Answers are still forthcoming. Researchers have not yet looked for myelin changes in older animals. Other experiments suggest myelination continues into our mid-50s but on a much subtler level.

Certainly white matter is key to types of learning that require prolonged practice and repetition, as well as extensive integration among greatly separated regions of the cerebral cortex. Children whose brains are still myelinating widely find it much easier to acquire new skills than their grandparents do. For a range of intellectual and athletic abilities, if an individual wants to reach world-class level he or she must start young. You built the brain you have today by interacting with the environment while you were growing up and your neural connections were still myelinating. You can adapt those abilities in many ways, but neither you nor I will become a world-class pianist, chess player or tennis pro unless we began our training when we were children.

Of course, old geezers can still learn, but they are engaged in a different kind of learning involving the synapses directly. And yet intensive training causes neurons to fire, so the potential exists for that firing to stimulate myelination.

Perhaps someday, when we fully understand when and why white matter forms, we can devise treatments to change it, even as it grows old. To deliver on that speculation, we would need to find the signal that tells an oligodendrocyte to myelinate one axon and not another one nearby. That discovery, buried deep underneath the gray matter, awaits unearthing by future explorers. "

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T:yksi ajatus

Pentti Haikonen järjestää ensi viikolla Helsingissä tapaamisen konetietoisuudesta: http://research.nokia.com/node/704. Suomen tekoälyseuran puheenjohtaja Tapani Raiko mainosti vielä tänään, että

Viesti tuli meille seuran jäsenille, mutta näköjään mukaan pääsee muutkin. Eihän tuo hinta ihan halpa tosiaan ole edes jäsenille, mutta ajattelin käydä katsastamassa.

Osaisitko sanoa perstuntumalta, miten Haikosen teoria suhtautuu edellä Scientic American 3/2008:sta lainaamaani R Douglas Fieldsin teoriaan?

Fieldsin teoria ainakin sopii täydellisesti yhteen pavlovilaisen ehdollistumisen teorian kanssa.

Samoin se natsaa hyvin yhteen Ehdollistumisen biokemiallisen mekanismin kanssa Bruce Catersonin mukaan.

Mutta on ehdotoman sovittamattomassa ristiriidassa esimerkiksi Kai Kailan/Matt Ridleyn, Riitta Harin/Giacomo Rizzolattin/Alvin Goldmannin, Antti Revonsuon tai Steven Pinkerin teorioiden kanssa.

Fieldsin teoria on julkaistu jo v. 2004, mutta se on nyt tarkentunut ja vahvistunut kehittyneimmillä aivokuvantamismenetelmillä.

Opiskelijoille 110 euroa. Hitto tuonnehan olisi melkein voinut mennä, tosin hintaan pitää laskea junaliput mukaan. Kerro meille köyhille mistä jäimme paitsi jälkeen päin.

The Other Half of the Brain.

Fields, R. Douglas

MOUNTING EVIDENCE SUGGESTS THAT GLIAL CELLS, OVERLOOKED FOR HALF A CENTURY, MAY BE NEARLY AS CRITICAL TO THINKING AND LEARNING AS NEURONS ARE

The recent book Driving Mr. Albert tells the true story of pathologist Thomas Harvey, who performed the autopsy of Albert Einstein in 1955. After finishing his task, Harvey irreverently took Einstein's brain home, where he kept it floating in a plastic container for the next 40 years. From time to time Harvey doled out small brain slices to scientists and pseudoscientists around the world who probed the tissue for clues to Einstein's genius. But when Harvey reached his 80s, he placed what was left of the brain in the trunk of his Buick Skylark and embarked on a road trip across the country to return it to Einstein's granddaughter.

One of the respected scientists who examined sections of the prized brain was Marian C. Diamond of the University of California at Berkeley. She found nothing unusual about the number or size of its neurons (nerve cells). But in the association cortex, responsible for high-level cognition, she did discover a surprisingly large number of nonneuronal cells known as glia--a much greater concentration than that found in the average Albert's head.

An odd curiosity? Perhaps not. A growing body of evidence suggests that glial cells play a far more important role than historically presumed. For decades, physiologists focused on neurons as the brain's prime communicators. Glia, even though they outnumber nerve cells nine to one, were thought to have only a maintenance role: bringing nutrients from blood vessels to neurons, maintaining a healthy balance of ions in the brain, and warding off pathogens that evaded the immune system. Propped up by glia, neurons were free to communicate across tiny contact points called synapses and to establish a web of connections that allow us to think, remember and jump for joy.

That long-held model of brain function could change dramatically if new findings about gila pan out. In the past several years, sensitive imaging tests have shown that neurons and glia engage in a two-way dialogue from embryonic development through old age. Glia influence the formation of synapses and help to determine which neural connections get stronger or weaker over time; such changes are essential to learning and to storing long-term memories. And the most recent work shows that gila also communicate among themselves, in a separate but parallel network to the neural network, influencing how well the brain performs. Neuroscientists are cautious about assigning new prominence to glia too quickly, yet they are excited by the prospect that more than half the brain has gone largely unexplored and may contain a trove of information about how the mind works.
See Me, Hear Me

THE MENTAL PICTURE most people have of our nervous system resembles a tangle of wires that connect neurons. Each neuron has a long, outstretched branch--an axon--that carries electrical signals to buds at its end. Each bud emits neurotransmitters--chemical messenger molecules--across a short synaptic gap to a twig like receptor, or dendrite, on an adjacent neuron. But packed around the neurons and axons is a diverse population of glial cells. By the time of Einstein's death, neuroscientists suspected that glial cells might contribute to information processing, but convincing evidence eluded them. They eventually demoted glia, and research on these cells slid into the backwater of science for a long time.

Neuroscientists failed to detect signaling among glia, partly because they had insufficient technology analytical but primarily because they were looking in tie wrong place. They incorrectly assumed that if glia could chatter they would use the same electrical mode of communication seen in neurons. That is, they would generate electrical impulses called action potentials that would ultimately cause the cells to release neurotransmitters across synapses, igniting more impulses in other neurons. Investigators did discover that glia had many of the same voltage-sensitive ion channels that generate electrical signals in axons, but they surmised that these channels merely allowed glia to sense indirectly the level of activity of adjacent neurons. They found that glial cells lacked the membrane properties required to actually propagate their own action potentials. What they missed, and what advanced imaging techniques have now revealed, is that glia rely on chemical signals instead of electrical ones to convey messages.

Valuable insights into how glia detect neuronal activity emerged by the mid-1990s, after neuroscientists established that glia had a variety of receptors on their membranes that could respond to a range of chemicals, including, in some cases, neurotranimitters. This discovery suggested that glia might communicate using chemical signals that neurons did not recognize and at limes might react directly to neurotransmitters emitted by neurons.

To prove such assertions, scientists first had to show that glia actually do "listen in" on neuronal communication and take action based on what they "hear'" Earlier work indicated that an influx of calcium into glial cells could be a sign that they had been stimulated. Based on that notion, investigators devised a laboratory method called calcium imaging to see whether glial cells known as terminal Schwann cells--. which surround synapses where nerves meet muscle cells--were sensitive to neuronal signals emitted at these junctions. The method confirmed that Schwann Cells, at least, did respond to synaptic firing and that the reaction involved an influx of calcium ions into the cells.

But were glia limited only to eavesdropping on neuronal activity, by scavenging traces of neurotransmitter leaking from a synapse? More general-function Schwann cells also surround axons all along nerves in the body, not just at synapses, and oligodencrocyte glia cells wrap around axons in the central nervous sys-tern (brain and spinal cord). At my National Institutes of Health lab, we wanted to know if glia could monitor neural activity anywhere as it flowed through axons in neural circuits. If so, how was that communication mediated? More important, how exactly would glia be affected by what they heard?

To find answers, we cultured sensory neurons (dorsal root ganglion, or DRG, cells) from mice in special lab dishes equipped with electrodes that would enable us to trigger action potentials in the axons. We added Schwann cells to some cultures and oligodendrocytes to others.

We needed to tap independently into the activity of the axons and the glia to determine if the latter were detecting the axon messages. We used a calcium-imaging technique to record visually what the cells were doing, introducing dye that fluoresces if it binds to calcium ions. When an axon fires, voltage-sensitive ion channels in the neuron's membrane open, allowing calcium ions to enter. We would therefore expect to see the firing as a flash of green fluorescence lighting up the entire neuron from the inside. As the concentration of calcium rose in a cell, the fluorescence would get brighter. The intensity could be measured by a photomultiplier tube, and images of the glowing cells could be digitized and displayed in pseudocolor on a monitor in real time--looking something like the radar images of rainstorms shown on weather reports. If glial cells heard the neuronal signals and did so in part by taking up calcium from their surroundings, they would light up as well, only later.

Staring at a computer monitor in a darkened room, my NIH colleague, biologist Beth Stevens, and I knew that after months of preparation our hypothesis was about to be tested with the flick of a switch. When we turned on the stimulator, the DRG neurons responded instantly, changing from blue to green to red and then white on a pseudocoior scale of calcium concentration,as calcium flooded into the axons.Initially,there were no changes in the Schwann cells or oligodendrocytes, but about 15 long seconds later the glia suddenly began to light up like bulbs on a string of Christmas lights [see illustration on page 59]. Somehow the cells had detected the impulse activity in the axons and responded by raising the concentration of calcium in their own cytoplasm.

Gila Communicating with Glia

THUS FAR WE HAD confirmed that gila sense axon activity by taking in calcium. In neurons, calcium activates enzymes that produce neurotransmitters. Presumably, the influx in glial cells would also activate enzymes that would marshal a response. But what response was the cell attempting? More fundamentally, what exactly had triggered the calcium influx?

Clues came from previous work on other gliai cells in the brain known as astrocytes. One of their functions is to carry nutrients from capillaries to nerve cells; another is to maintain the optimal ionic conditions around neurons necessary for firing impulses. Part of the latter job is to remove excess neurotransmitters and ions that neurons release when they fire. In a classic 1990 study, a group led by Stephen J. Smith of Yale University (now at Stanford University) used calcium imaging to show that the calcium concentration in an astrocyte would rise suddenly when the neurotransmitter glutamate was added to a cell culture. Calcium waves soon spread throughout all the astrocytes in the culture. The astrocytes were responding as if the neurotransmitter had just been released by a neuron, and they were essentially discussing the news of presumed neuronal firing among themselves.

Some neuroscientists wondered whether the communication occurred because calcium ions or related signaling molecules simply passed through open doorways connecting abutting astrocytes. In 1996 S. Ben Kater and his colleagues at the University of Utah defused that suspicion. Using a sharp microelectrode, they cut a straight line through a layer of astrocytes in culture, forming a cell-free void that would act like a highway separating burning forests on either side. But when they stimulated calcium waves on one side of the break, the waves spread to astrocytes across the void with no difficulty. The astrocytes had to be sending signals through the extracellular medium,rather than through physical contact.

Intensive research in many laboratories over the next few year! showed similar results. Calcium responses could be induced in astrocytes by adding neurotransmitters or by using electrodes to stimulate the release of neurotransmitters from synapses. Meanwhile physiologists and biochemists were finding that glia had receptors for many of the same neurotransmitters neurons use for synaptic communication, as well as most of the ion channels that enable neurons to fire action potentials.

ATP Is the Messenger

THESE AND OTHER RESULTS led to confusion. Glial communication is controlled by calcium influxes just as neuronal communication is. But electrical impulses trigger calcium changes in neurons, and no such impulse exists in or reaches glia. Was glial calcium influx initiated by a different electrical phenomenon or some other mechanism?

In their glial experiments, researchers were noticing that a familiar molecule kept cropping up--ATP (adenosine triphosphate), known to every biology student as the energy source for cellular activities. Although it makes a great power pack, ATP also has many features that make it an excellent messenger molecule between cells. It is highly abundant inside cells but rare outside of them. It is small and therefore diffuses rapidly, and it breaks down quickly. All these traits ensure that new messages conveyed by ATP molecules are not confused with old messages. Moreover, ATF is neatly packaged inside the tips of axons where neurotransmitter molecules are stored; it is released together with neurotransmitters at synapses and can travel outside synapses, too.

In 1999 Peter B. Guthrie and his colleagues at the University of Utah shouted conclusively that when excited, astrocytes release ATP into their surroundings. The ATP binds to receptors on nearby astrocytes, prompting ion channels to open and allow an influx of calcium. The rise triggers ATP release from those cells, setting off a chain reaction of AT mediated calcium responses across the population of astrocytes.

A model of how glia around an axon sense neuronal activity and then communicate to other glia residing at the axon's synapse was coming together. The firing of neurons somehow induces glial cells around an axon to emit ATP, which causes calcium intake in neighboring glia, prompting more ATP release, thereby activating communication along a string of glia that can reach far from the initiating neuron. But how could the glia in our experiment be detecting the neuronal firing, given that the axons made no synaptic, connections with the glia and the axonal gila were nowhere near the synapse? Neurotransmitters were not the answer; they do not diffuse out of axons (if they did, they could act in unintended places in the brain, wreaking havoc). Perhaps ATP, which is released along with neurotransmitters when axons fire, was somehow escaping along the axon.

To test this notion, we electrically stimulated pure cultures of DRG axons and then analyzed the medium. By exploiting the enzyme that allows fireflies to glow--a reaction that requires ATP--we were able to detect the release of ATP from axons by seeing the medium glow when axons fired. We then added Schwann cells to the culture and measured the calcium responses. They also lit up after axons fired an action potential. Yet when we added the enzyme apyrase, which rapidly destroys ATP-thereby intercepting the ATP before it could reach any Schwann cells--the glia remained dark when axons fired. The calcium response in the Schwann cells had been blocked, because the cells never received the ATP message.

ATP released from an axon was indeed triggering calcium influx into Schwann cells. Using biochemical analysis and digital microscopy, we also showed that the influx caused signals to travel from the cells' membrane to the nucleus, where the genes are stored, causing various genes to switch on. Amazingly, by firing to communicate with other neurons, an axon could instruct the readout of genes in a glial cell and thus influence its behavior.

Axons Control Glia's Fate

TO THIS POINT, work by us and others had led to the conclusion that a glial cell senses neuronal action potentials by detecting ATP that is either released by a firing axon or leaked from the synapse. The gliai cell relays the message inside itself via calcium ions. The ions activate enzymes that release ATP to other glial cells or activate enzymes that control the readout of genes.

This insight made us wonder what functions the genes might be controlling. Were they telling the glia to act in ways that would influence the neurons around them? Stevens set out to answer this question by focusing on the process that prompts production of the myelin insulation around axons, which clearly would affect a neuron. This insulation is key to the conduction of nerve impulses at high speed over long distances. Its growth enables a baby to gradually hold up its head, and its destruction by diseases such as multiple sclerosis causes severe impairment.

We turned to myelin because we were curious about how an immature Schwann cell on an axon in the peripheral nervous system of a fetus or infant knows which axons will need myelin and when to start sheathing those axons and, alternatively, how it knows if it should transform itself into a cell that will not make insulation. Generally, only large-diameter axons need myelin. Could axon impulses or ATP release affect these decisions? We found that Schwann cells in culture proliferated more slowly when gathered around axons that were firing than around axons that were quiet. Moreover, the Schwann cells' development was arrested and myelin formation was blocked. Adding ATP produced the same effects.

Working with Vittorio Gallo and his colleagues in the adjacent NIH lab, however, we found a contrasting situation with the oligodendrocyte glia that form myelin in the brain. ATP did not inhibit their proliferation, but adenosine, the substance left when phosphate molecules in ATP are removed, stimulated the cells to mature and form myelin. The two findings indicate that different receptors on glia provide a clever way for a neuron to send separate messages to glial cells in the central or peripheral nervous system without having to make separate messenger molecules or specify message destinations.

Better understanding of myelination is important. Every year thousands of people die and countless more are paralyzed or blinded because of demyelinating disease. Multiple sclerosis, for example, strikes one in 700 people. No one knows what exactly initiates myelinadon, but adenosine is the first substance derived from an axon that has been found to stimulate the process. The fact that adenosine is released from axons in response to axon firing means activity in the brain actually influences myelination. Such findings could mark paths to treatment. Drugs resembling adenosine might help. Adding adenosine to Stem cells could perhaps turn them into myelinating gila that are transplanted into damaged nerves.

Outside the Neuronal Box

EXPERIMENTS IN OUR LAB and others strongly suggest that ATP and adenosine mediate the messages coursing through networks of Schwann and oligodendrocyte gila cells and that calcium messages are induced in astrocyte glia cells by ATP alone. But do glia have the power to regulate the functioning of neurons, other than by producing myelin?

The answer appears to he "yes." Richard Robitaille of the University of Montreal saw the voltage produced by synapses on frog muscle become stronger or weaker depending on what chemicals he injected into Schwann cells at the synapse. When Eric A. Newman of the University of Minnesota touched the retina of a rat, waves of calcium sent by glia changed the visual neurons' rate of firing.Studying slices of rat brain taken from the hippocampus --a region involved in memory-- Maiken Nedergaard of New York Medical College observed synapses increase their electrical activity when adjacent astrocytes stimulated calcium waves. Such changes in synaptic strength are thought to be the fundamental means by which the nervous system changes its response through experience--a concept termed plasticity, suggesting that glia might play a role in the cellular basis of learning.

One problem arises from these observations. Like a wave of cheering fans sweeping across a stadium, the calcium waves spread throughout the entire population of astrocytes. This large-scale response is effective for managing the entire group, but it cannot convey a very complex message. The equivalent of "Go team!" might be useful in coordinating general activity in the brain during the sleep-wake cycle or during a seizure, but local conversations are necessary if glial cells are to be involved in the intricacies of information processing.

In a footnote to their 1990 paper, Smith and his colleagues stated that they believed neutrons and glia carried on more discrete conversations. Still, the researchers lacked experimental methods precise enough to deliver a. neurotransmitter in a way that resembled what an astrocyte would realistically experience at a synapse. In 2003 Philip G. Haydon of the University of Pennsylvania achieved this objective. He used improved laser technology to release such a small quantity of glutamate in a hippocampal brain slice that t would be detected by only a single astrocyte. Under this condition, Haydon observed that an astrocyte sent specific calcium signals to just a small number of nearby astrocytes. As Haydon put it, in addition to calcium waves that affect astrocytes globally, "there is short-range connectivity between astrocytes."

In other words, discrete astrocyte circuits in the brain coordinate activity with neuronal circuits. (The physical or biochemical factors that define these discrete astrocytic circuits are unknown at present.) Investigation by others has also indicated that astrocytes may strengthen signaling at synapses by secreting the same neurotransmitter the axon is releasing--in effect, amplifying the signal.

The working hypothesis that Haydon and I, along with our colleagues, are reaching from these discoveries is that communication among astrocytes helps to activate neurons whose axons terminate relatively far away and that this activity,in turn,contributes to the release of neurotransmitters at distant synapses. This action would regulate how susceptible remote synapses are to undergoing a change in strength, which is the cellular mechanism underlying learning and memory.

Results announced at the Society for Neuroscience's annual meeting in November 2003 support this notion and possibly expand the role of glia to include participation in the formation of new synapses [see box on opposite page]. Some of the findings build on research done two years earlier by Ben A. Barres, Frank W. Pfrieger and their colleagues at Stanford, who reported that rat neurons grown in culture made more synapses when in the presence of astrocytes.

Working in Barres's lab, postdoctoral students Karen S. Christopherson and Erik M. U1lian have subsequently found that a protein called thrombospondin, presumably from the astrocyte, was the chemical messenger that spurred synapse building. Thrombospondin plays various biological roles but was not thought to be a major factor in the nervous system. The more thrombospondin they added to the astrocyte culture, though,the more synapses appeared. Thrombospondin may be responsible for bringing together proteins and other compounds needed to create a synapse when young nerve networks grow and therefore might contribute to the modification of synapses as the networks age.

Future experiments could advance our emerging understanding of how glia affect our brains. One challenge would be to show that memory--or a cellular analogue of memory, such as long-term potentiation--is affected by synaptic astrocytes. Another challenge would be to determine precisely how remote synapses might be influenced by signals sent through astrocyte circuits.

Perhaps it should not be surprising that astrocytes can affect synapse formation at a distance. To form associations between stimuli that are processed by different circuits of neurons-the smell of a certain perfume, say, and the emotions it stirs about the person who wears it--the brain must have ways to establish fast communication between neuronal circuits that are not wired together directly, if neurons are like telephones communicating electrically through hardwired synaptic connections, astrocytes may be like cell phones, communicating with chemical signals that are broadcast widely but can be detected only by other astrocytes that have the appropriate receptors tuned to receive the message. If signals can travel extensively through astrocyte circuits, then glia at one site could activate distant gila to coordinate the firing of neural networks across regions of the brain.

Comparisons of brains reveal that the proportion of glia to neurons increases greatly as animals move up the evolutionary ladder. Haydon wonders whether extensive connectivity among astrocytes might contribute to a greater capacity for learning. He and others are investigating this hypothesis in new experiments. Perhaps a higher concentration of glia, or a more potent type of glia, is what elevates certain humans to genius. Einstein taught us the value of daring to think outside the box. Neuroscientists looking beyond neurons to see how glia may be involved in information processing are following that lead.

MORE TO EXPLORE

Driving Mr. Albert: A Trip across America with Einstein's Brain. Michael Paterniti. Delta, 2001.

New Insights into Neuron-Glia Communication. R. D. Fields and B. Stevens-Graham in Science, Vol. 298, pages 556-562; October 18, 2002.

Adenosine: A Neuron-Glial Transmitter Promoting Myelination in the CNS in Response to Action Potentials. B. Stevens, S. Porta, L. L. Haak, V. Gallo, and R. D. Fields in Neuron, Vol. 36, No. 5, pages 855-868; December 5, 2002.

Astrocytic Connectivity in the Hippocampus. Jai-Yoon Sul, George Orosz, Richard S. Givens, and Philip G. Haydon in Neuron Glia Biology, Vol. 1, pages 3-11; 2004.

Also see the journal Neuron Glia Biology:
http://www.journals.cambridge.org/jid%5fNGB

Overview/Glia

• For decades, neuroscientists thought neurons did all the communicating in the brain and nervous system, and glial cells merely nurtured them, even though glia outnumber neurons nine to one.

• Improved imaging and listening instruments now show that glia communicate with neurons and with one another about messages traveling among neurons. Glia have the power to alter those signals at the synaptic gaps between neurons and can even influence where synapses are formed.

• Given such prowess, glia may be critical to learning and to forming memories, as well as repairing nerve damage. Experiments are getting under way to find out.

PHOTO (COLOR): GLIAL CELLS outnumber neurons nine to one in the brain and the rest of the nervous system.

PHOTO (COLOR): GLIA AND NEURONS work together in the brain and spinal cord. A neuron sends a message down a long axon and across a synaptic gap to a dendrite on another neuron. Astrocyte gila bring nutrients to neurons as well as surround and regulate synapses. Oligodendrocyte gila produce myelin that insulates axons. When a neuron's electrical message [action potential] reaches the axon terminal [inset], the message induces vesicles to move to the membrane and open, releasing neurotransmitters [signaling molecules] that diffuse across a narrow synaptic cleft to the dendrite's receptors. Similar principles apply in the body's peripheral nervous system, where Schwann cells perform myelination duties.

PHOTO (COLOR): ASTROCYTES REGULATE SIGNALING across synapses in various ways. An axon transmits a signal to a dendrite by releasing a neurotransmitter (green)--here, glutamate. It also releases the chemical ATP [gold]. These compounds then trigger an influx of calcium (purple) into astrocytes, which prompts the astrocytes to communicate among themselves by releasing their own ATP. Astrocytes may strengthen the signaling by secreting the same neurotransmitter, or they may weaken the signal by absorbing the neurotransmitter or secreting proteins that bind to it (blue), thereby preventing it from reaching its target. Astrocytes can also release signaling molecules I red) that cause the axon to increase or decrease the amount of neurotransmitter it releases when it fires again. Modifying the connections among neurons is one way the brain revises its responses to stimuli as it accumulates experience--how it learns. In the peripheral nervous system, Schwann cells surround synapses.

PHOTO (COLOR): MOVIE MADE using scanning-laser confocal microscopy [later colorized] shows that glial cells respond to chattering neurons. Sensory neurons [two large bodies, 20 microns in diameter] [al and Schwann glial cells [smaller bodies] were mixed in a lab culture containing calcium ions [invisible J. Dye that would fluoresce if calcium ions bound to it was introduced into the cells. A slight voltage applied to the neurons prompted them to fire action potentials down axons [long lines], and the neurons immediately lit up [bl, indicating they had opened channels on their membranes to allow calcium to flow inside. Twelve seconds later [c}, as the neurons continued to fire, Schwann cells began to light up, indicating they had begun taking in calcium in response to the signals traveling down axons/Eighteen seconds after that [d], more gila had lit up, because they had sensed the signals. The series shows that gila tap into neuronal messages all along the lines of communication, not just at synapses where neurotransmitters are present.

PHOTO (COLOR): HOW DO GLIA communicate? Gila called astrocytes [a] and sensory neurons [not shown] were mixed in a lab culture containing calcium ions. After a neuron was stimulated to fire action potentials down long axons [lightning bolts] [b], gila began to light up, indicating they sensed the message by beginning to absorb calcium. After 10 and 12.5 seconds [c and d], huge waves of calcium flux were sweeping across the region, carrying signals among many astrocytes. Green to yellow to red depicts higher calcium concentration.

Katselin eilen taivaalle ja huomasin, että elokuu on taas tuonut tähdenlennot mukanaan, näin kaksi.

Mietin edelleen noita ulottuvuusjuttuja ja mieleeni tuli karmaiseva ajatus.

Mitä jos ihmisen kyky muistaa ja kuvitella asioita onkin vain kykyä nähdä toisiin ulottuvuuksiin? Periaatteessahan muistaminen ja kuvitteleminen ovat nimenomaan sitä, mitä "korkeammissa" ulottuvuuksissa on: kaikki eri ajanhetket ja mahdolliset lopputulokset eri tapahtumille.

Olisiko niin, että ihmiset elävätkin jo kaikessa kymmenessä ulottuvuudessa, mutta fyysisesti olemme jumissa kolmessa "pienimmässä" ulottuvuudessa, ajan töniessä meitä jatkuvasti eteenpäin, halusimme tai emme.

Terra Cognitalta tulossa taas kiintoisan oloinen teos. En löytänyt kyllä vielä omilta sivuiltaan vaan 3 sepän kirjakaupasta:

Marco Iacoboni: Ihmisten peilaus. Kytkeytymisemme uusi tiede
230 s. 35 € -

Kurkkasin Iacobonin esitelmän JuuTjuubista. Ei mitään ihmeellistä uutta, mutta ihan hyvä esitys. Minusta oleellisin asia oli, että MI totesi peilisolujen olevan liikkeiden abstrakteja esityksiä. Sinänsä ei siis sekään mitään ihmeellistä eikä uutta, mutta asian saisi minusta sanoa ääneen useammin. Useinhan nämä peilisolut esitetään jotenkin kauhean poikkeuksellisina, mutta täytyyhän aivoista löytä jos jonkinlaiselle abstraktiolle herkkiä hermosoluja. Hämmästyttävämpää olisi, jos aivoissa ei olisi yhtään hermosolua, joka reagoi liikkeen tai intention abstraktille ajatukselle.


Koitan ehtiä... Onko jotain erityistä, mistä haluaisit kuulla?

Kaikkihan tuossa listassa vaikuttaa mielenkiintoiselta. Osaat varmaan poimia asiantuntijana kaikkein uusimmat ja merkittävimmät tutkimustulokset.

Iacobonin "teoria" tiedetään: syntyessään vanhentunutta jankutusta:

http://www.vapaa-ajattelijat.fi/keskust ... #msg-18798

"SARJASSAMME ”EUROTIEDE” TÄNÄÄN:

“PEILISOLU” ON PSYKOLOGIASSA TURHA JA HARHAANJOHTAVA KÄSITE

Tiede 8/2005 –lehti kirjoittaa ihmisen aivokuoren oletetuista geneettisesti toiminnallisesti erikoistuneista neuroneista (hermosoluja) otsikolla ”Peilisolut auttavat ymmärtämään muita”.1 Liekö koskaan väitetty missään muualla kuin ”peilisoluteoriassa”, että ´ymmärtäminen´ olisi solutason ilmiö. Kansan Ääni on aikaisemmin käsitellyt ”peilisoluteoriaa” otsikolla ”Europuoskaritiedettä Suomen tieteen huippuyksikössä”.2

Vaikka Tiede-lehden artikkelissa jo mainitaankin ehdollistumisteoria, toisin kuin ainakaan suomalaisten ”peilisoluista” kirjoittaneiden aikaisemmissa esityksissä, niin uuden kirjoituksen perusteella ei näytä olevan aihetta tarkistaa tuolloin esittämääni tyrmäävää arviota peilisoluteorian järkevyydestä ja todenperäisyydestä.

Erityisistä ”peilisoluista” on tämän ”euroteorian” mukaan määritelmällisesti kyse, jos jokin aivokuoren alue osoittaa magneettikuvauksessa aktivoitumista sekä jotakin tiettyä toimintoa itse suoritettaessa että havaittaessa muiden suorittavan sitä.

Välittömästi herää ensinnäkin kysymys, mistä on ”päätetty”, että kyseessä olisi nimenomaan solutason ilmiö. ”Perusteluksi” ei kelpaa sellainen latteus, että ”aivot koostuvat neuroneista” (paitsi korkeintaan jonkin höpötiedelehden poliittisessa jutussa!), sillä neuronien välillä on myös rakenteita, ja erilaistumattomienkin neuronien keskinäiset tilapäisetkin kytkennät voivat kantaa vaikka kuinka monimutkaista informaatiota. Tieteessä EI saisi tehdä perustelemattomia yleisyyttä rajoittavia olettamuksia: silloin helposti osa koetulosten varteenotettavista mahdollisista selityksistä sivuutetaan perusteettomasti, jolloin tutkimus on väärin suoritettu.

Ilmeisesti ”peilisolu”-termin isä Giacomo Rizzolatti mittasi solutason ilmiöitä alun perin nobelisti ja Nobel-komitean puheenjohtaja Ragnar Granitin Helsingin yliopistossa 40-luvulla kehittämällä elektrodimenetelmällä havaitessaan kokeellisesti ”peilaamiseksi” tulkitsemansa ilmiön, joka sivumennen sanoen ainakin muilta kuin sen ”solutason” osalta on pilkulleen samanlainen kuin mitä vallitseva I.P.Pavlovin ehdollistumisteoriakin ennustaa ilman minkäänlaisia ”peili-” tai muita erikoistuneita neuroneja ainakaan aivokuorella!

Otaniemen kylmälaboratorion aivotutkimusyksikön magneettikuvaus ei menetelmänä ulotu solutasolle (ei erottele solu- ja niiden välisen tason ilmiöitä). Rizzolattin makakeilla suorittamia kokeita ei tuossa suhteessa ole myöskään pystytty toistamaan muilla lajeilla, eivätkä näiden kaikki pöytäkirjat ole edes ”sosiobiologistikirkon” napamiesten/naisten saatavilla.8 ”Solutaso” onkin asetettu siellä ”omienkin” keskuudessa kyseenalaiseksi, samoin ns. tietoisuuden simulaatuoteoria, jonka mukaan ”tajunta tulisi peilisolusta” vähän niin kuin jokin molekyyliparvi…8 "

" Peilisoluteoreetikkojen nykyisestä käsityksestä peilisoluteorian ja ehdollistumisteorian keskinäisestä suhteesta ”Tieteen” artikkeli lainaa kahta vähemmän esillä ollutta tutkijaa:

” - Toisten ymmärtäminen todella vaikuttaa niin yksinkertaiselta, että asiaa on vaikea uskoa. Ei tässä silti ole mitään mystistä. Periaatteessa tämä on klassista ehdollistumista, Christian Keysers sanoo.

– Käyttäytyminen on valtaosin liikkeitä, eleitä ja ilmeitä, ja ihminen oppii ihmisen tavoille sosiaalisessa kanssakäymisessä ja paljolti muita matkimalla. Jäljittely, joka alkaa lähes heti syntymän jälkeen, valmentaa aivot tuntemaan ja tunnistamaan niin omia kuin toisten olotiloja, Marco Iacoboni täydentää. ” 1

Iacoboni on valinnut tarkoin sanansa: hänen mukaansa (esimerkiksi) jäljittely ja siihen liittyvä (toiminnon) palkitseminen/palkkiutuminen/palkittuminen eivät LUO niitä "omia ja toisten (psyykkisiä) olotiloja" (kuten tapahtuu instrumentaalisen ehdollisen refleksin muodostuessa!), vaan matkiminen "valmentaa tunnistamaan" jotkin psyykkiset ilmiöt, jotka "jo ovat", ilmeisestikin jonkinlaisten "potentioiden" ominaisuudessa (vähän niin kuin ylikiltin vanhanpiian orgasmi, joka ei ole koskaan "saanut", vaikkei asialle mitään ylitsekäymätöntä fysiologista estettä olisikaan...)

Varmasti OSA aivokuvantamisessa ilmenevistä aivokuoren pinnan alueiden aktivoitumisista todellakin liittyy klassisiin ehdollisiin reflekseihin. Iacoboni tietää aivan oikein, että ”hänen tavallaan” opitaan nimenomaan klassisia ehdollisia refleksejä, tietoisesti tai tiedostamattomasti. Mutta ei instrumentaalisia.

Mutta klassistenkaan ehdollisten refleksien olemassaolo ei todista minkäänlaisten geneettisten ”peilisolujen” olemassaolosta aivokuorella.

Päinvastoin, myös klassisten ehdollisten refleksien tähänastinen teoria kieltää aivokuoren pinnan geneettisesti erikoistuneiden neuronien/alueiden olemassaolon, vähintäinkin tarpeettomina, ellei suorastaan vahingollisina organismin tehokkaan ympäristöönä sopeutumisen kannalta! (Sikäli Keysers joko valehtelee, puhuu ristiin tai ei pidä itsekään ”peilisolujaan/alueitaan” ”suoraan geenistä” erikoistuneina, vaan niiden alapuolisten alueiden erikoitumisen heijastumina. SE taas ei olisi ristiriidassa klassisten ehdollisten refleksien ominaisuuksien kanssa.) "

" Se tarkoittaa sitä, että erilaiset toiminnot (refleksien reaktio-osat), joilla on ”peilialue” (ei kinata nyt yksityiskohdista…), esimerkiksi sormen koukistaminen, ovat muka geneettisesti määrytyneitä. Tuo toiminto sitten havaitaan sekä itsellä että muilla ja todetaan ”samaksi”. Toiminnan mielikuva itse kullakin viittaa ennen kaikkea omaan ko. toimintaan, mutta koska nuo (”alkeis”?)toiminnot ovat eri henkilöillä muka ”Keenistä” osapuilleen samoja, niin ihmiset muka tietäisivät toiminnan perusteella myös erittäin luotettavasti, mitä muut ajattelevat, tai miltä heistä tuntuu!

Ehdollistuminen ja oppiminen tunnustetaan sanoissa, mutta funktionaalisesti (ja myös evolutionaarisesti vaikuttavana olennaisena ”ympäristötekijänä” organismille 10) niiden olemassolo ja vaikutus kielletään niin kuin ennenkin. ”Kaikki tulee keenistä”, hokevat ”peilisoluteoreetikot” yhä, vain hieman toisin sanoin.

Suunnattoman paljon yksinkertaisempaa ja monissa tapauksissa ainoa mahdollisuus on olettaa, että toimintamme varsinaisena perustana (ja myös korkeimpien nisäkkäiden ja lintujen toiminnan perustana, ja myös ihmisen kielen representoitumisen mekanismina) toimivat instrumentaaliset eivätkä klassiset ehdolliset refleksit!

Esimerkiksi nuo tarttumarefleksit ovat aivan varmasti juuri niitä, ja ihmisellä ne ovat lisäksi kielellis-ajatuksellisesti muokattuja, mikä ilmenee aivojen ns. Brocan kielialueen aktivoitumisena ihmisen niitä niin suorittaessa kuin havainnoidessakin!

Ehdollistumisteoriassa tarvita ensimmäistäkään spesialisoitunutta ”peilisolua”, kun taas peilisoluteoria ei kuitenkaan pärjää ilman ehdollistumista! Tieteenfilosofinen ns. ”Occamin partaveitsi” -periaate määräisi tällöin pysyttäytymään ehdollistumisteoreettisessa selittämisessä (vähintäänkin kunnes ilmenisi jotakin, mitä se ei kerta kaikiaan selitä!) "

" ”Peilisoluteoria” on katsottava nykyisellään kuuluvaksi ”evoluutiopsykologisten” eli ”sosiobiologisten” teorioiden ryhmään, joihin sisältyy väärä ja älytön olettamus ”geenistä tulevasta ajattelusta”. "

Kannattaa lukea tämä artikkeli, ja säästää rahansa.

Riitta Hari ehti muuten "julkistaa peilisolut" Suomessa Luonnonfilosofisen (hörhö)seuran esitelmätilaisuudessa noin vuosi ennen R. Douglas Fieldsin ensimmäisen artikkelin oilmestymistä Scientific American 4/2004:ssa. Mutta MIKSI juuri hörhöseurassa?

http://keskustelu.skepsis.fi/html/Kesku ... iID=113022

Oliko joku kieltänyt julkistamasta "tuloksiaan" yliopiston virallisissa tilaisuuksissa?

Mitä väliä, minkä seinien suojassa tuloksensa julkaisee? Olennaistahan on, että tiedeyhteisön jäsenet (joihin RJK tuntuu lukevan myös itsensä) voivat tutustua päättelyn kulkuun ja perusteisiin sekä esittää kommenttinsa ja kritiikkinsä.

Ei se varsinaisesti olemuksellista olekaan.

On hyvä, että suuri yleisö saa välillä nähdä sellsitakin tieteentekoa lainaumerkeissä ja ilman, jota yliopistonjohto ei olisi lennosta valmis päästämään julkisuuteen.



Niihin pitää päästä kaikkien tutustumaan, jotka kynnelle kykenevät.

Päivystävä dosentti pyysi minua kirjoittamaan tänne. Workshoppi oli siis Pentti Haikosen järjestämä ja hän oli itse kutsunut kaikki puhujat. Netistä löytyy lista esitelmistä ja puhujista: http://www.conscious-robots.com/en/publ ... -step.html
Pidin itse esitelmän otsikolla The engine of thought - a bio-inspired mechanism for distributed selection of useful information.

Kiinnostavimpia esitelmiä pitivät omasta mielestäni Ron Chrisley, Ben Goertzel, Will Browne ja Igor Aleksander. Jälkimmäinen piti 45 min johdantoesityksen, jossa ei sinänsä tullut mitään ihmeellistä uutta ainakaan minulle (olen lukenut Igorin kirjoja ja kuullut hänen esitelmiään ennenkin), mutta alustuksena esitys oli erinomainen. Erityisen hyviä pointteja Aleksanderilla oli siihen, miksi ihmisten on niin vaikea yhdistää sanoja "kone" ja "tietoisuus". Oma taustani on koneoppiminen, neuroverkot, matematiikka, neurofysiologia, ... Minulle on ihan tuttua, että kone voi oppia ja havaita tai että sillä voi olla uskomuksia, päämääriä, emootiota, tunteita, merkityksiä jne. Silti minunkin on vaikea asettua tällaisen koneen asemaan ja pohtia miltä koneesta tuntuu.

Germund Hesslow oli tapaamisen ainoa aivotutkijaksi luokiteltava esiintyjä. Itse esitelmä ei ollut kovin ihmeellinen (käsitteli sitä, miten periaatteessa aivojen on mahdollista simuloida maailmaa), mutta keskustelin hänen kanssaan väliajoilla hänen pikkuaivotutkimuksestaan. Olen itse soveltanut pikkuaivojen toimintaperiaatetta robottien ohjauksessa ja juttua siis riitti. Hesslow valitteli sitä, että monet pikkuaivotutkijatkaan eivät (vielä?) tiedä, miten pikkuaivot toimivat, vaikka kokeellista evidenssiä on vaikka millä mitalla. (Tarkoitan nyt pääperiaatteita, en jokaisen hermosolun ja synapsin tarkkoja mekanismeja.) Jos sattuu kiinnostamaan, asiaan voi tutustua vaikka tuolta: http://www.lce.hut.fi/~harri/irto/ (ensimmäinen osa tekstimuodossa, kalvot ja videot).

Oman esitykseni pointteja olivat: 1) Jos aivojen toimintaa haluaa ymmärtää, on tärkeää tutkia neuraalisen "implementaatiotason" (synapsit, neuronit, välittäjäaineet, ionikanavat, ...) ja käyttäytymisen tason (käyttäytyminen, mieli, tietoisuus, ...) väliin jäävää informaation prosessoinnin tasoa. Tämä helpottaa neuronien toiminnan ja käyttäytymisen tason ilmiöiden välisten yhteyksien hahmottamista. 2) Aivojen informaationkäsittelyn ymmärtämiseksi on hyödyllistä tutkia niitä ongelmia, joita aivot ovat kehittyneet ratkomaan (tietenkin sen lisäksi, että tutkitaan kokeellisesti aivojen mekanismeja). 3) Esitin kokeellisesti havaittujen mekanismien pohjalta rakennetun aivokuoren mallin, jossa valikoiva tarkkaavaisuus ja abstraktien neuraalisten representaatioiden oppiminen emergoituu verrattain yksinkertaisista mekanismeista. Lisätietoa täältä: http://www.lce.hut.fi/~harri/publicatio ... pola08nwmc

Ron Chrisley piti esitelmän, joka pyrki kattamaan hyvin paljon asioita (30 min loppui pahasti kesken monelta muultakin kuin minulta ja Ronilta). Ronin tärkein pointti oli, että aivokuoren representaatiot eivät kuvaa pelkästään sitä, mitä maailmassa havaitaan, vaan sitä, mitä maailmassa havaittaisiin, jos tehtäisiin sitä tai tätä. Esimerkki: näköaivokuori ei representoi pelkästään sitä, mitä retinalla näkyy, vaan sitä, mitä retinalla näkyisi, jos silmää liikutettaisiin sinne tai tänne. Tämä selittäisi monia havaintopsykologian löytämiä (hämmentäviä?) ilmiöitä. Esimerkiksi sen, että sokean täplän kohdalla näköjärjestelmä keksii kuvalle sopivan jatkumon. Chrisleyn kuvaaman kaltaisia ennustavia representaatiota on sovellettu myös "insinöörien" toimesta koneoppimisessa. Esim: http://www.cs.ualberta.ca/~sutton/publi ... NetOptions
Chrisley nosti esille myös sen, mihin konetietoisuutta tutkimalla pyritään. Konferenssissa esitettiin sekä tutkimusta, jonka tärkeimpänä tavoitteena on tietoisuuden tuottaminen koneisiin (esimerkiksi jotta ne pärjäisivät paremmin monimutkaisissa tehtävissä ja ympäristöissä), että tutkimusta, jonka tavoitteena on ihmisten tietoisuuden ymmärtäminen mallintamisen kautta. Ronin kotisivut: http://www.cogs.susx.ac.uk/users/ronc/

Ben Goertzelin käsitys tietoisuudesta oli minusta vähintäänkin omintakeinen: tietoisuutta on joka paikassa himppusen. Benin tärkein anti olikin minusta lähinnä hänen tekoälytutkimuksensa, joka on minusta kunnianhimoisuudessaan tervetullut poikkeus keskimääräiseen nykymenoon (useimmiten ratkotaan yksittäisiä ongelmia; unelma yleisestä tekoälystä on monissa piireissä ainakin toistaiseksi hylätty). Lisää vaikka tuolta: http://en.wikipedia.org/wiki/Ben_Goertzel

Will Browne (http://www.personal.rdg.ac.uk/~sis01wnb/wnb/wnb.htm) puhui emootioista ja tunteista. Kaiketi tämä on Damasion jako: emootiot ovat tämän määritelmän mukaan ruumiillisia reaktioita ja tunteet ovat näiden havaitsemista ja ymmärtämistä (eli näköjärjestelmä havaitsee, mitä retinalle tulee; tunnejärjestelmä havaitsee, mitä emootioita elimistö tuottaa; nämä ovat myös kytköksissä siten, että elimistö tuottaa emootioita tunnejärjestelmän reaktioiden pohjalta). Brownen pointti oli, että emootiot ovat käyttäytymisen ohjauksen kannalta hyödyllisiä. Hän esitteli koetuloksia, joissa robotti pystyi selviytymään (yksinkertaisesta) tehtävästä paremmin, kun ohjausjärjestelmä perustui emootioihin. Samanlaisia ideoita ovat totta kai esittäneet muutkin (muistaakseni esimerkiksi Paul Verschure), mutta liian usein minusta emootiot on roboteissa jätetty pinnalliselle tasolle. Niiden tarkoitus on silloin vain tuottaa ihmiselle tunne robotin tunteista, vaikka niitä ei ulkokuoren takana ole. Brownen robotilla oli ihan ihka oikeat emootiot, vaikka ne olivatkin yksinkertaiset eikä robotilla ollut riittävästi aivoa ymmärtää omia emootioitaan (jos minä sen Damasion määritelmän siis ymmärsin, robotilla oli emootioita, mutta ei tunteita).

Yhteenvetona: tapasin muutaman hyvin mielenkiintoisen tutkijan, mutta mitään ihmeellistä uutta en tainnut tietoisuudesta oppia. Minusta kehitys menee eteenpäin sillä, että selvitetään vielä tarkemmin aivojen informaationkäsittelyä ja rakennetaan ja tutkitaan samoilla periaatteilla toimivia oppivia ja älykkäitä robotteja. Siinä sivussa opitaan varmasti yhtä jos toistakin tietoisuudesta, mutta ei se ainakaan minulla ole tutkimusta ajava päämäärä.