In:
eLife, eLife Sciences Publications, Ltd, Vol. 4 ( 2015-11-26)
Kurzfassung:
When part of the brain becomes damaged as a result of injury or disease – for example, a stroke – other brain regions can sometimes take over from the damaged part. This is one example of a phenomenon called brain plasticity. The strengthening and weakening of connections between neurons that underlies learning and memory is another, less extreme, example of plasticity. While the brain is most plastic during childhood, it remains malleable to some degree throughout life. The brain’s visual system in particular shows robust and predictable plasticity, and so is often used by neuroscientists to study mechanisms behind plasticity. In young rodents, taping one eye shut for a few days causes inputs from that eye to visual areas of the brain to become weaker. Inputs from the open eye meanwhile become stronger, leading to improved vision in the open eye. Such plasticity also occurs in adult rodents, but the eye must be closed for longer to produce an effect. In young animals, this plasticity depends, in part, on enzymes called matrix metalloproteinases (MMPs). These help to regulate a network of proteins called the extracellular matrix, which provides structural support for cells. Pielecka-Fortuna et al. now provide the first evidence that MMP enzymes also contribute to visual plasticity in adult animals. Blocking the activity of MMPs prevented reorganisation of visual areas of the brains of adult mice in response to eye closure, and prevented vision improvements in the open eye. However, blocking MMP in adult mice whose brains had been damaged by a stroke had the opposite effect. Whereas stroke normally prevents visual system plasticity in response to eye closure, treatment with a single dose of MMP blocker rescued this plasticity. Strikingly, these benefits were lost if the mice were given two doses of MMP blocker, rather than one. These experiments show that MMP levels must be within a narrow range to support plasticity. In the healthy adult brain, blocking MMPs impairs plasticity. After stroke, MMP levels are increased and reducing them rescues plasticity. The next challenge is to identify the specific MMP enzymes responsible, and to determine whether these changes can be exploited to improve recovery from stroke.
Materialart:
Online-Ressource
ISSN:
2050-084X
DOI:
10.7554/eLife.11290.001
DOI:
10.7554/eLife.11290.002
DOI:
10.7554/eLife.11290.003
DOI:
10.7554/eLife.11290.004
DOI:
10.7554/eLife.11290.005
DOI:
10.7554/eLife.11290.006
DOI:
10.7554/eLife.11290.007
DOI:
10.7554/eLife.11290.008
DOI:
10.7554/eLife.11290.009
DOI:
10.7554/eLife.11290.010
DOI:
10.7554/eLife.11290.011
DOI:
10.7554/eLife.11290.012
DOI:
10.7554/eLife.11290.013
DOI:
10.7554/eLife.11290.014
DOI:
10.7554/eLife.11290.015
DOI:
10.7554/eLife.11290.016
Sprache:
Englisch
Verlag:
eLife Sciences Publications, Ltd
Publikationsdatum:
2015
ZDB Id:
2687154-3
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