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The Brain What Happens to a Linebacker's Neurons?

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  • Paul Cannaday
    Title of Article:The Brain What Happens to a Linebacker s Neurons? The Disability Grapevine Online Newspaper:Issue #39 The Disability Grapevine Online World
    Message 1 of 1 , Sep 7, 2010
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      Title of Article:The Brain What Happens to a Linebacker's Neurons?
      The Disability Grapevine Online Newspaper:Issue #39
      The Disability Grapevine Online World Newspaper
      Tuesday, September 07, 2010
      Year 10
      ****The Number One Daily Newspaper for People with Disabilities****
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      Just Ask Paul Questions, email Paul at Disablenet@...
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      Submitted by:
      "Roxie Mayfield & Jade in beautiful Eugene, Oregon "

      Article:
      The Brain What Happens to a Linebacker's Neurons?
      http://discovermagazine.com/2010/jul-aug/18-brain-what-happens-to-a-lineback
      ers-neurons/
      by Carl Zimmer
      From the July-August special issue; published online August 18, 2010

      A blow to the head can change the neural architecture of the brain from
      elastic to brittle, with devastating consequences.

      Every spring the National Football League conducts that most cherished of
      American rituals, the college draft. A couple of months before the event,
      prospective players show off their abilities in an athletic audition known
      as the combine. Last winter's combine was different from that of previous
      years, though. Along with the traditional 40-yard dashes and bench presses,
      the latest crop of aspirants also had to log time in front of a computer,
      trying to solve a series of brainteasers. In one test, Xs and Os were
      sprinkled across the computer screen as the athletes took a test that
      measured how well they could remember the position of each letter. In
      another, words like red and blue appeared on the screen in different
      colors. The football players had to press a key as quickly as possible if
      the word matched its color.

      These teasers are not intended to help coaches make their draft picks. They
      are for the benefit of the players themselves-or, to be more precise, for
      the benefit of the players' gray matter. Under pressure from Congress, the
      N.F.L. is taking steps to do a better job of protecting its players from
      brain damage. The little computer challenges that the draft candidates had
      to solve measure some of the brain's most crucial functions, such as its
      ability to hold several pieces of information at once. Given the nature of
      football, it is extremely likely that a number of this year's draft picks
      will someday suffer a head injury on the field. After that happens, N.F.L.
      doctors will give them the same tests again. By comparing the new results
      with the baseline scores recorded just before the draft, the doctors will
      get a clearer sense of how badly the football players have damaged their
      brains and what degree of caution to take during recovery.

      The N.F.L.'s sudden interest in neuroscience is just the latest sign that
      we, as a society, are finally taking brain injuries more seriously. It's
      about time. Neurologists estimate that every year more than a million
      people suffer brain injuries in the United States alone-not just from
      football mishaps, but also from car crashes, falls down stairs, and many
      other kinds of accidents. And that figure is probably a serious
      underestimate, because many brain injuries go undiagnosed. It is easy to
      believe that if you feel fine after a fall, then you must truly be fine,
      but even so-called mild brain injuries can have devastating consequences.
      People's personalities may shift so they can no longer hold down their job
      or maintain their marriage. Sometimes "mild" brain injuries even lead to
      dementia.

      This hidden epidemic of brain injury is not only tragic but also strange
      and mysterious. Brains don't fail in obvious ways, as bones do when they
      snap or skin does when it rips. Scientists are only now starting to
      discover the subtle damage that occurs when the brain is injured: It gets
      disturbed down to its individual molecules.

      The brain floats in a sealed chamber of cerebrospinal fluid, like a sponge
      in a jar of water. If you quickly sit down in a chair, you accelerate your
      brain. The force you generate can cause it to swirl around and shift its
      shape inside the braincase. The brain is constantly twisting, stretching,
      and squashing within your head. Given the delicacy of the organ-a living
      brain has the consistency of custard-it is amazing that we manage to get to
      the end of each day without suffering severe damage.

      Douglas Smith, director of the Center for Brain Injury and Repair at the
      University of Pennsylvania, has been running experiments for the past
      decade to understand how we are able to survive such regular assaults.
      Smith builds miniature brains by growing live rat neurons on a stretchable
      membrane attached to a custom-built metal plate. Roughly the size of a
      postage stamp, the plate is lined with microscopic grooves crossing a
      flexible strip of silicone that runs across the middle. As the neurons grow
      on each side, they sprout long branches, called axons, which creep down the
      grooves to make contact with neurons growing on the other side in order to
      transmit electric signals between them.

      Once the axons have matured, Smith and his colleagues shoot the metal
      plates with carefully controlled puffs of air. They direct the puffs at the
      silicone strip, which stretches in response. In the process, the air
      delivers a sudden force to the axons as well. Smith and his colleagues then
      observe the axons to see how they handle the assault.

      It turns out that axons are remarkably elastic. They can stretch out slowly
      to twice their ordinary length and then pull back again without any harm.
      Axons are stretchy due in part to their flexible internal skeleton. Instead
      of rigid bones, axons are built around structural elements, mostly bundles
      of filaments called microtubules. When an axon stretches, these
      microtubules can slide past one another. If the movement is gradual, the
      microtubules will immediately slide back into place after the stretching
      stops, with no harm done.

      If Smith delivers a quick, sharp puff of air, however, something else
      entirely happens. Instead of recoiling smoothly, the axon develops kinks.
      Over the next 40 minutes, the axon gradually returns to its regular shape,
      but after an hour a series of swellings appears. Each swelling may be up to
      50 times as wide as the normal diameter of the axon. Eventually the axon
      falls apart.

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      http://discovermagazine.com/2010/jul-aug/18-brain-what-happens-to-a-lineback
      ers-neurons/article_view?b_start:int=1&-C=

      These kinks form, Smith believes, when microtubules are stretched so
      rapidly that they snap. The broken filaments can no longer slide neatly
      back over one another and instead bunch up, causing the kinks. Normally,
      enzymes inside neurons are constantly taking apart microtubules and
      building new ones with the recycled parts. But now the enzymes attack the
      broken ends of the microtubules, causing the internal structure of the axon
      to dissolve. With the microtubules turning to mush, the axon begins to
      relax and lose its kinks. The axons look fairly normal, but they are
      catastrophically damaged.

      Microtubules do more than give neurons their structure. They also serve as
      a kind of cellular railway network. Proteins travel from one end of a
      neuron to the other by moving along microtubules. If microtubules break,
      the result is much like what happens when a railroad track is damaged. The
      proteins pile up, and these traffic jams produce the swellings in the axons
      that Smith sees in his experiments. The swellings get so big that they
      eventually rupture, tearing the axon apart and spewing out damaged proteins.

      Smith's findings could shed light on a common but puzzling brain trauma
      known as diffuse axonal injury. This happens when people experience sudden
      accelerations to the brain-from a bomb's shock waves, for example, or from
      whiplash in a car crash. Very often the acceleration causes people to lose
      consciousness. In serious cases it can lead to trouble with cognitive
      tasks, such as deciding whether the word red is actually printed in red.
      When pathologists perform autopsies on people with diffuse axonal injury,
      they see severed axons with swollen tips, just like what Smith sees in his
      experiments.

      Smith's research also suggests that even mild shocks to the brain can cause
      serious harm. If he hit his axons with gentle puffs of air, they didn't
      swell and break. Nevertheless, there was a major change in their molecular
      structure. Axons create the electric current that allows them to send
      signals by drawing in positively charged sodium ions*. A moderate stretch
      to an axon, Smith recently found, causes the sodium channels to
      malfunction. In order to keep the current flowing, the traumatized axons
      start to build more channels.

      Smith suspects that such a mended axon may be able to go on working, but
      only in a very frail state. Another stretch-even a moderate one-can cause
      the axon to go haywire. Its additional sodium channels now malfunction, and
      the axon tries to compensate by creating even more channels. But these
      channels are now so defective that they start letting in positively charged
      calcium ions. The calcium atoms activate enzymes that destroy the gates
      that slow the flow of sodium through the channels, so now even more sodium
      rushes in-and then more calcium, in a runaway feedback loop. The axon dies
      like a shorted-out circuit.

      This slower type of axon death may happen when someone suffers mild but
      repeated brain injuries, exactly the kind that football players experience
      as they crash into each other in game after game. Cognitive tests like the
      ones at this year's N.F.L. combine can pinpoint the mental troubles that
      come with dysfunctional or dying axons. There is precious little research
      to indicate how long a football player should be sidelined in order to let
      his brain recover, though, and Smith's experiments don't offer much
      comfort. Preliminary brain studies show that axons are still vulnerable
      even months after an initial stretch.

      Once a person does sustain a brain injury, there is not a lot doctors can
      do. They can open a hole in the skull if pressure in the brain gets too
      high. But they have no drugs to treat the actual damage. Some 30 compounds
      have made it into phase 3 trials in humans, only to fail.

      The latest research could point scientists to more effective treatments.
      Smith, for example, recently found that the anticancer drug taxol can
      stabilize the microtubules in neurons, protecting them from catastrophic
      disassembly after a sharp shock. Now that we know the damage to the brain
      happens at the molecular level, we may find a cure for the injured brain
      waiting there as well.

      * Correction, August 23, 2010: This sentence originally referred to
      "negatively charged sodium atoms."

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