Results 1 to 3 of 3

Thread: Regeneration versus plasticity

  1. #1

    Regeneration versus plasticity

    There is some misunderstanding concerning what regeneration and plasticity in the central nervous system. I thought that I would articulate what I think the two phenomena are and see if they fit other people's perceptions.

    Regeneration. The term regeneration when used in biology refers to "regrowth of lost or destroyed parts or organs" . The definition indicates "parts". Thus, an axon is part of a neuron. The neuronal cell located in the brain or the spinal cord respectively send axons down or up the spinal cord. Injury damages the axon. The part of the axon that is still attached to the cell body survives although it may die back from the injury site for a short distance. However, the part of the axon that is separated from the cell body by the injury will die. Therefore, in order to regenerate, the neuron must regrow the axon from the point of dieback across the injury site and back to where it originally conneccted with another neuron. Because of their axons, neurons are by far the largest cells of the body. For example, a neuron situated in the dorsal root sensory ganglia has two axons, one of which goes peripherally to innervate sensory receptors and the other one goes centrally into and up the spinal cord to the brain where it connects to neurons in the brainstem and thalamus. Axons grow relatively slowly (about 1 mm per day, probably no faster than hair growth). Depending on the distance of the growth, regeneration may take a months or even years.

    Plasticity. In biology, this word usually refers to capability to build or form tissues. In neuroscience, however, this word has a more specific meaning. It refers to the ability of the nervous tissues to form new connections. When the spinal cord is injured, many axons are disconnected from neurons above or below the spinal cord. Disconnection of axons from cells is sometimes called denervation. Denervation vacates synaptic sites, the places where axons connect to other neurons or muscle. Many studies have shown that local axons will rapidly sprout and connect to vacated synaptic sites within days. This is a form of plasticity. Recently, Martin Schwab showed that the antibody IN-1, which blocks the growth inhibiting molecule Nogo on myelin, will stimulate sprouting of axons in the spinal cord. For example, when he cuts half of the spinal cord and applies IN-1 to the spinal cord, he and his colleagues have found that IN-1 stimulates surviving corticospinal axons to sprout. This may account for the recovery that he has observed in the spinal cord. Likewise, several groups have recently reported that chondroitinase ABC (ChaseABC) will also stimulate sprouting and plasticity in the brain and spinal cord. Since chondroitinase is an enzyme that breaks down an extracellular matrix protein called chondroitin sulfate proteoglycan (CSPG) that is known to inhibit axonal growth, many people have hypothesized that CSPG (like Nogo) may inhibit plasticity or sprouting in the spinal cord.

    Regeneration differs from plasticity in that regeneration requires regrowth of an axon back towards its original target. Plasticity implies the sprouting of axons to connect to neurons that they did not connect to before or at least not as much. The latter requires some surviving axons but does not require long-distance regrowth of axons. The former requires regrowth of injured axons back towards or to their original targets.

    Wise.

  2. #2
    excellent, i had thought regeneration and plasticity were loosely the same thing before reading your post. am i correct in saying that we have some control over plasticity (fueled by things such as treadmill training, UBE time and/or intensive exercise) but so far no control of regeneration (with the exception perhaps being stem cell transplants)?

    if that is true would i also be correct that any gains we might make in plasticity (controlled progress) stand in addition to nerve regeneration (uncontrolled progress), assuming there were some way to measure what was contributing what to recovery?

    i've also had plasticity explained to me as the moldability of the muscle, is that right?

    thanks wise

    noah

  3. #3
    Originally posted by buckwheat:

    excellent, i had thought regeneration and plasticity were loosely the same thing before reading your post. am i correct in saying that we have some control over plasticity (fueled by things such as treadmill training, UBE time and/or intensive exercise) but so far no control of regeneration (with the exception perhaps being stem cell transplants)?

    if that is true would i also be correct that any gains we might make in plasticity (controlled progress) stand in addition to nerve regeneration (uncontrolled progress), assuming there were some way to measure what was contributing what to recovery?

    i've also had plasticity explained to me as the moldability of the muscle, is that right?

    thanks wise

    noah
    Buckwheat, the word plasticity certainly does apply to muscles. Muscles are among the most "plastic" of the tissues that we have in our body. They are constantly remodelling themselves iin response to exercise or lack of exercise. What people really did not realize until perhaps a decade or two ago is how malleable the spinal cord is and how it participates in muscle plasticity. It is now clear that inactivity of muscles not only lead to atrophy of the muscles but changes in the circuitry of the spinal cord. The recent work showing that exercise can restore function of long-inactive motor systems has been truly eye-opening. Of course, there is a lot of work going on in the brain that suggests that all parts of the central nervous system are "plastic", including places that we would never think about. But, the data has been staring us in the face for many decades. It is only that we have been blind to it. For example, recently studies indicate that the somatosensory and visual cortices (two physically separated and distinctly different functions of the brain) appear to be able to swap functions and support each other. Likewise, studies of children who have lost half of their brain (due to hemispherectomy) suggest that the remaining half of the brain can take over functions of the lost half of the brain. Finally, certain neural circuits that I would have thought are completely hardwired turn out to be very plastic. This includes the circuits that mediate our eye movements and neck movements.

    The work of Blair Calancie reported at the recent meeting in Biloxi brought this subject to mind. He essentially showed that a majority of people with chronic spinal cord injury develop aberrant connections that grow in reliability and tightness with time after injury, so that stimulation of the leg will produce consistent movements of the hands. Other people have been reporting a variety of strange connectivity going from the back to the leg, sacrum to the shoulders, etc., etc. Most of these phenomena are likely to be related to plasticity. How much may be related to spontaneous regeneration is unclear but I think that if so much plasticity is possible, we should not be ruling out regeneration either.

    Wise.

Posting Permissions

  • You may not post new threads
  • You may not post replies
  • You may not post attachments
  • You may not edit your posts
  •