Neuroplasticity

Is the nervous system flexible or inflexible?

Playing football in New Zealand (yes, football, not rugby) can be dangerous. In a match of staff against students I was once knocked out for a short time by a clumsy player whose boot hit my head. Immediately thereafter I could not see with my right eye and that worrying condition remained until gradually my vision returned. Now, this does not have much to do with the topic of this essay, “neuroplasticity”, because the photoreceptors in my eye and the neurons in my brain that process the visual information were not destroyed. But had they been, what would have happened?

You probably learnt at school that cells of the nervous system cannot regenerate and that established neuronal connections cannot be altered. As examples for the irreversible damage affecting the nervous system, paraplegia and quadriplegia are cited. However, although research on spinal cord damage and restoring functionality in humans have not yet led to any breakthroughs, Purves et al. of the Washington School of Medicine could show in the mid 1980s that one and the same neuron in a mouse’s nervous system was involved for two weeks or more in remodelling beyond the usually considered developmental period. This suggested that rearrangements were possible well into mouse’s adult life. The fate of the neuron was not fixed: a case, therefore, of neuroplasticity.

Another example: connections between the eyes and the brain are far from fixed at birth not only mice but humans too. A baby’s eye’s resolution is improving dramatically within the first six months of a baby’s life. This is partially due to an increase of receptor cells in the eye’s fovea. Other changes affect the speed with which the visual information reaches the brain, involve the coating with myelin of the nerve fibres and the establishment (or de-establishment) of synapses (= contact points) between neurons. The increase and decrease of synapses is not genetically programmed and which of them remain and which disappear depends largely on the visual experience in early infanthood.

The visual system is not “rigid”, but “plastic”. Some brain cells are already in contact with the two eyes at birth; others, however, are not yet determined and a competition for “vacancies” ensues between the two eyes. This form of neuroplasticity makes sense, because the connections of the binocular nerve cells to the two eyes could not possibly be working accurately if hard-wired at birth. If one eye, its cornea or lens, the attached muscles, etc. would only be slightly different from the pre-programmed positioning, binocular vision would no longer be accurate. Therefore, the observed neuroplasticity allows for adjustments. In fact should one eye be blind or suffering from cataract at birth, then the non-determined visual cells in the brain can switch and contact only the healthy, seeing eye during the critical first few months post-partum. Whether such flexibility lasts at least to a small extent into the adult life of humans is not fully known, but there is a chance.

We tend to take “seeing” for granted and assume it’s there instinctively, but an element of “learning to see” very definitely is contributing. Kittens, for example, raised to look at an environment consisting only of either horizontal or vertical striped cylinders later exhibit severe visual handicaps. It therefore seems that fixing a “mobile” above our baby’s cot, perhaps, had a more useful function than just being decorative: it helped baby learn to see!

eye discovery pond snail photoreceptor

Turn your mind upside-down with this article !

© Dr V.B. Meyer-Rochow and http://www.bioforthebiobuff.wordpress.com, 2017.
Unauthorized use and/or duplication of this material without express and written permission from this site’s author and/or owner is strictly prohibited. Excerpts and links may be used, provided that full and clear credit is given to V.B Meyer-Rochow and http://www.bioforthebiobuff.wordpress.com with appropriate and specific direction to the original content

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