Chronicles in Science: Synaptic Plasticity (56K, go away)

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Chronicles in Science: Synaptic Plasticity (56K, go away)

Post by Fire Fly » 2008-06-28 06:17am

Chronicles in Science: Synaptic Plasticity

So now that school has come to a halt and I having not much to do, I thought it a good idea to share some of the things that I’ve learned over the years. I’m hoping that this will be the first in a series of science articles on different topics such as neuroscience, genetics, physiology, biochemistry, and other such topics that the greater population may not be aware of. I’m hoping to discuss things that people would generally not know about unless they’ve taken a university course on it or have read science papers. Hopefully, for the interested reader, this will provide a small foundation and some direction about where to look online if you find this interesting. As a side note, there may be some inaccuracies but that may be due to the fact that I've had to skip over lots and lots of details to make most of this understandable to those who may not have had extensive backgrounds in biology.

In this first article, I will be focusing on neuroscience. Normally, one would start with cellular and molecular neuroscience but I figure that if I want to keep people’s attention, I’ll start with the more interesting stuff. This first article will focus on synaptic plasticity (adapted from the slides of Professor Tom Yin) and the second article will likely focus on neuroethology.

So what is plasticity? Well, here is a common phenomenon that all of us are aware of: speaking with accents. People who immigrate to the US and who eventually learn to speak fluent English will speak English with an accent that is reflective of their native country whereas people who are born in the US or who immigrate to the US at a very early age, they speak English that is relatively accent free. When I mean accent, I do not mean a Boston accent or a Midwestern accent (with respect to the United States); I’m talking about speaking English with a Chinese accent or a Pakistani accent. This phenomenon is illustrated in the follow graph:

Image


As you can see, there is something that is happening in our brains at a very early age that does not happen at a much later age.

Another example of plasticity from our motor system; this shows axons innervating muscle fibers:

Image

Neuroscientists know that in mature adult nervous systems, each muscle fiber is innervated by a single axon (an axon is a nerve bundle that allows signals to be transmitted). Now each axon innervates many muscle fibers in general due to the innervation ratio, which depends on the characteristic of the motor neuron. What sets this innervation ratio? The size of the fiber will matter but how does the muscle ‘know’ the size of the neuron? The muscle “knows” because of the activity type of the muscle, whether the muscle is phasic or tonic (i.e. muscles that are for force and muscles for maintaining posture, respectively). This single neuronal innervation occurs in mature systems but at birth, each muscle fiber is poly-neuronally innervated; several different axons may innervate a single muscle fiber. So somewhere in between development, we have elimination of the extra axons, often referred to as synapse elimination, so that in the end each fiber is innervated by only a single axon. Why is this important at all? It’s important for control. In order to have fine motor control, you want controlled input into these fibers; you don’t want multiple signals coming in telling the muscle to do several different things. Moreover, if each muscle is innervated by only one axon, then suddenly whole groups of muscles can be controlled independently of one another allowing you to activate one particular muscle and not activate all the others. This is a common developmental phenomenon. What underlies this developmental phenomenon? Many neuroscientists think that this involves a competitive process called Hebbian learning.

So how do scientists study this developmental phenomenon?

Image

There are several different ways but one of the classic ways in the visual system is to inject the eye with a tridiated amino acid (radioactive); these amino acids will become incorporated into proteins. These proteins will then be transported down the axons from the eye to the brain by anterograde transport down the axon where they will synapse with a brain structure called the lateral genucliate nucleus (LGN). When the tridiated amino acids reached the LGN, they are transported again from the LGN to the visual cortex. If you look at a particular layer of the visual cortex (Layer IV; the visual cortex is organized into multiple layers from Layer I to Layer VI) you can see a reflection of that radioactivity coming from one eye ball. Another method is to use horseradish peroxidase, a staining compound.

So when you look at the visual cortex, what you will actually see are stripes, called ocular dominance columns. Each stripe corresponds to a layer of cells that are receiving visual input via axons from one eye and another stripe corresponds to a layer of cells that are receiving visual input from another eye (in the picture below, the dark stripes might correspond to cells that are receiving visual input from the left eye while the non-dark stripes might be cells that are receiving visual input from the right eye). The following experiments that will be described were performed in kittens in layer IV of the visual cortex (layer IV has cells that receive input from one eye or the other only, monocular vision, where as the other layers, such as layers I, II, III, V, and VI, receive input from both eyes, binocular vision).


Image

So how does plasticity apply to these eye experiments? Hubel and Weise, the people who originally studied these particular phenomenon, monocularly deprived kittens during the 1st year of their life so that only one eye was receiving visual input. Then they injected the normal eye (after the kittens were sacrificed, of course) to see what happened in the visual cortex and what they saw was that the ocular dominance columns changed considerably where the seeing eye “took over” much of the cortical area. In the following picture, you can see that the dark stripes (the deprived eye) are considerably weak compared to the light stripes (the seeing eye).


Image

In normal development, one typically observes ocular dominance columns that are of equal width:

Image

The small circles indicate that those cells show some changes; they shrink but they don’t disappear completely. By suturing one eye shut, you don’t deprive the eye completely; you only deprive most of the light. So the reflection of this abnormal input from the right eye (see above picture) causes a change in the cortex where the two eyes start to come together. Naturally, you might expect that these anatomical changes are a reflection of the physiological changes.

So here’s an experiment that summarizes everything that they saw:

Image

While they were recording from the different cells of the visual cortex, for each cell, along with figuring out all the different properties of the visual cells, the cells were tested to see if they were driven by the left eye, by the right eye, or by both. They then rated the cells (1 through 7) by a histogram; a lower number indicated that the cell was driven more preferentially by one eye (let’s say the left eye) and a higher number indicated that the eye was driven more preferentially by the other eye (let’s say the right). If the cell was driven equally by both eye (binocular cell), then the cell was put into the middle of the histogram. As you can imagine, most cells are binocular but there are a few that are monocular.

In a normal cats, there is a normal histogram; very few of the cells are non-responsive (see above image, left). If the eye was shut from birth to 2.5 months and then waited for the 3rd year to do the actual experiment (see above image, middle), what happens? Well, there is a disappearance of responsiveness of the cells from the sutured eye; all of the cells were driven by only the seeing eye. So the kitten was deprived of light in one eye for a period of 2.5 months and then allowed to see normally and even thought it could see normally, there was a dramatic change in its cortical anatomy to the point that the seeing eye completely took over, that is, all of the visual cells were receiving input only from the seeing eye. This is very strong evidence of the critical period phenomenon; something happened in these first 2 months that completely changed the visual system.

What happens if you do this experiment in adults (see above image, right)? Adult kittens were allowed to see normally for the first year of its life. At the end of first year, one eye was shut and kept so for 2 years; after the 2 year period, the visual cortex was analyzed. But what we see is that there has been no major change, we only see more or less normal ocular dominance columns with a slight reduction in the number of cells that are binocular and monocular. So as said, something really strange happens in the first few months of the kitten’s life (hint: critical period).

So what exactly is this critical period? Well, in another experiment to better understand this critical period, the animal was deprived of light for 3 days after one year from birth and other animals deprived for 6 days after one year from birth.


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Right away, we see a strong abnormality after only 3 days of deprivation; with a 6 day deprivation, all of the cells are driven by only the seeing eye. As you can imagine, this has some clinical significance. A few decades ago, people tried to correct strabismus (where the two eyes are not aligned properly) by weakening one eye to make them align. The work just shown shows that such clinical practices must be made very, very carefully or otherwise, you could essentially blind a person in one eye.

As mentioned before, this pruning of synapses is called Hebbian learning. In 1949, a man by the name of Donald Hebb proposed a mechanism for this synaptic plasticity: synapses are strengthened by coincident activation of pre-synaptic and post-synaptic cell. So if a cell receives a pre-synaptic input, that synapse and the cell will be strengthened if they are coincidently activated and those which are not that case will be relatively weaken. The actual mechanism of this mechanism is due to a particular receptor, NMDA receptors (will discuss another time, just take my word for now or see Wikipeida for a general idea of what I’m talking about).

So how does Hebbian learning affect monocular deprivation? The open eye will be able to detect light and will fire signals and the neighboring cells will also fire, causing similar firing activity. The coincident activation of neighboring synapses will cause the post-synaptic cell to be depolarized. The covered eye, however, will detect some light and will fire in a more random pattern. In short, cells that fire together wire together; cells which fire more and fire together will be more useful versus cells that fire less and do not fire together. The nervous system can detect which nerves are firing more often and which nerves are firing less often and will prune away those which are not working as much as those which are.


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How does Hebbian learning affect behavior? In the next example, the barn owl is used to study this particular phenomenon by studying the visual and auditory system of the barn owl. The barn owl is able to hunt in complete darkness by using its auditory localization to help it; of course, its visual system can also be used when it doesn’t hunt at night. In the optic tectum of the barn owl (the human equivalent is the superior colliculus), there is visual input from the retinas and input from the auditory system. These inputs form a topographic map in the owl’s tectum. These topographic maps are reflective of the physical environment.


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If auditory input that is coming from directly ahead it will input into the same part of the optic tectum that is receiving visual input from straight ahead. If auditory input is coming from twenty degrees to the right, the visual information from degrees to the right will input into the same part of the owl’s tectum as the auditory information. So we see here that visual and auditory information from the same spatial location are inputted into the same part of the brain; they’re in alignment. This convergence in the optic tectum of the auditory and visual map helps the owl to cross reference visual information and auditory information in its brain to be a more effective hunter, particularly at night.


Image

If you record from cells in the optic tectum and as you go down into the deeper layer, you can find cells that are driven by both auditory and visual inputs. If you compare the visual receptive field (shown by the V in Figure A) with the auditory field (shown by the open circle in Figure A) with the square indicating the best area, you can see that the visual and auditory inputs are in alignment. How can this experiment be performed? Well, you have an anesthetized owl looking ahead at a screen and you shine light on the screen to determine what part of the screen excites what particular eye cell and then you have a speaker play a sound in the same location as the part of the screen to determine what part of the auditory field excites the cell and then you should be able to see that the visual cells which are responsive to one particular location and the auditory cells which are response to the same location are both in the same area of the owl’s brain.


ImageImage

So what a guy by the name of Eric Knudsen did was to ask what happens if you misalign these maps? He had the owls were prism glasses were prism glasses for 24 hours a day (image above, left) from a very young age. These prism glasses then deflect the visual field to the left or to the right. So if a mouse is ahead, the owl’s auditory input will tell the owl that the mouse is at zero degrees (directly ahead) but it’s visual input will tell the owl that the mouse is at 23 degrees to the left when the mouse is really 23 degrees to the right. So there is a discrepancy between the auditory and visual fields. So what happens in the behavior and physiology of the owl?


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What’s shown here are successive trials of a barn owl before the prisms are put on. The owl was trained to strike at auditory and visual targets and each dot represents one trial. When the owl is not wearing the prism, the owl accurately detects the visual and auditory target (a look alike mouse or a squeeking mouse). When the 23 degree prisms are placed on, the owl’s auditory targeting is fine but it’s visual targeting now has shifted by 23 degrees. The interesting thing is that after 42 days of training, we see that the owl’s auditory targeting has shifted so that it’s in alignment with its visual targeting. So even though the auditory fields are correct, after 42 days and the owl is still looking at 23 degrees to the right, there is an adaptation; of course, the discrepancy must be disconcerting for the owl, so its nervous system attempts to adapt to this apparent confusion. After the prisms are removed, the visual field becomes normal again and the owl is able to visually target accurately but its auditory targeting now is off by 23 degrees to the right. So what we see here is essentially a reprogramming in the owl’s brain.


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Picture above demonstrates the owl’s behavior due to the prism rearing.


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So that’s what happens behaviorally but what happens physiologically? As you can expect, during this period of adaptation, there is a shift of the auditory field to become in alignment with the visual field. This shows a drawing of the auditory and visual receptive field after several months of adaptation. As you can see, with the prisms on, the auditory and visual field is in alignment but with the prisms off, the original visual field goes back to normal and there is a misalignment. The vectors show responses from a given cell in the optic tectum and they all have this rightward vector which is approximately equal to the rightward deviation of the prism.


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So what’s the evidence for the critical period I’ve been talking about? In young owls, the adaptation occurs but in older owls, the adaptation does not occur. That is, in young owls, their nervous system is able to adjust their visual or auditory fields to be in alignment but in old owls, this does not happen. In order to make this plasticity occur in adult owls (it can occur), you need to let the adult owls hunt, that is, they must be actively using their vision and audition and this will allow some adaptation but it will not be nearly as dramatic as it is in young owls. We see this particular phenomenon in humans, particularly with respect to learning languages. When older people say it’s hard to learn a new language, there is truth to it; after so many years of speaking one particular language, it’s difficult for their brain to rewire itself to properly learn something drastically new and different.

As you can imagine, this synaptic plasticity phenomenon occurs in other sensory modalities also, not just vision and audition. The part of the brain which is responsible for touch sensation is the primary somatasensory cortex (S1). People have found that certain parts of S1 correspond to certain body parts. As you can imagine, certain body parts have a greater cortical representation than other parts; the more sensitive a particular body part is, the more brain space you need to process those touches. This particular phenomenon is illustrated in the homunculus below.


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So how does plasticity apply to our sensation of touch? Well, when people lose fingers (or other body parts), the cortical representation for that finger will be lost and the neighboring cortical representations for the other fingers will take over that lost finger’s cortical space. In following experiment, the middle finger of a monkey is amputated and the somatasensory cortex of the monkey was mapped and we see that after a period of time, the cortical area for digit 3 has been completely taken over by digit 2 and digit 4 (shown below). Why do we see this loss of cortical representation for the amputated finger? One particular reason is that with the finger now lost, you want to increase the sensitivity of the other fingers; as you can imagine, this has certain survival advantages. Another reason is simply due to Hebbian learning; the neurons are no longer firing to that particular cortical space and the nervous system simply prunes it away because it can no longer detect input. Why waste good resources?


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Other experiments have shown that specialized training of a monkey to use its finger in certain tasks will generate an expansion of the cortical representation. As you can see in the illustration below, a monkey was trained to perform a particular task using certain parts of its fingers, the area highlighted red or blue. After extensive training, the monkey’s S1 was mapped and the researchers found an expansion in the cortical representation. In Figure A (Control), we see that each digit has a part of the brain which corresponds to the distal part of the finger (the finger tips) or to the proximal part of the finger (near the palm). After training, we see that in Figure D, there has been an expansion. The dark red reads Digit 3 distal and the light red reads Digit 2 distal (the far end of the finger); the dark blue reads Digit 3 proximal and the light blue reads Digit 2 proximal (the part of the finger closer to the palm). So clearly, we see an expansion in the cortical representation of Digit 2 and Digit 3. As you can imagine, this is one reason why learning to play an instrument from an early age is better than learning to play at a later age; the younger the child, the better their brain can adapt to the specialized training whereas in adults, it takes considerable practice to get good at playing the piano or a violin because this synaptic plasticity effect is much weaker in adults.


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As you can see then, the early age of animals is an extremely crucial time period where the brain is maturing. It is during this early age that the brain is undergoing all sorts of rewiring and reconnecting, a period called the critical period and this particular phenomenon is called synaptic plasticity. These critical periods can influence behaviors in an extremely profound way from maternal bonding (i.e. baby geese) to learning languages. It may be easy to understand their behavioral effects but understanding the biological basis is rather difficult. What these experiments show is that simple experience can drastically influence the function and connectivity of neurons, leading to altered behaviors.

There is a whole lot more that I could talk about but this should be enough to wet your lips about the wonders of neuroscience. Stay tune for the next article where I discuss the bat brain.

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Post by Anguirus » 2008-06-28 10:31am

Cool! Thanks for posting this!
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Post by Fire Fly » 2008-06-28 03:34pm

Here's a nice video demonstration of what exactly Hubel and Weisel were doing with their visual experiments in kittens: youtube.

And if a mod could please fix the broken image link, that would be appreciated.

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Post by Ace Pace » 2008-06-29 03:40pm

Thats pretty damn awesome. One question though is whether any such expiriments are preformed on humans or is it simply too problematic (ethically, legally) to actually do any research there?
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Post by Fire Fly » 2008-06-29 03:45pm

Ace Pace wrote:Thats pretty damn awesome. One question though is whether any such expiriments are preformed on humans or is it simply too problematic (ethically, legally) to actually do any research there?
It can't be done in humans; the best you'll be able to do are non-invasive studies with imaging techniques or study in non-human primates.

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Re: Chronicles in Science: Synaptic Plasticity (56K, go away

Post by The Grim Squeaker » 2014-05-20 05:34am

By the Old Gods and the New - holy crap awesome. :D
While googling graphics for my current seminar in Neuroplasticity, I ended up here. (Yes, this is a hellacious thread necro. I think it's amusing enough, and I have stuff to add).

Just for now, (I'll return to this later), Some elaborations on what was written by Fire Fly :

On the topic of Critical Periods:
A few interesting asides are as follows:
  • We know that there are "Critical periods" (CP) for a number of cortical circuits/ mental functions, in various beasties (humans included. Cataracts in babies that aren't noticed will leave the child with visual deficits for life due to the lack of proper input).
    However! There are quite a number of senses and circuits that do not have a CP, and/or are not dependant on experience (~environmental input) in order to attain their "normative" function and wiring. That's maybe not that surprising, although it is quite speculative (We simply haven't been able to test everything yet). What is surprising however, is how different cortical functions may or may not be experience dependant (Yes, to anyone who knows much neurobiology, I'm butchering the term, pray forgive me) , depending on the organism in question, and that this also varies with the microcircuits involved. For example, Mice are born and their sense of smell WILL wire up and work (in general. There's always specifics to go over). Similarly, in insects (e.g. Drosophila), the neurons and circuits involved in flight will wire up correctly, even if they don't fly at all during their early development. On the other hand, Putting a kitten in a rotating basket shortly after birth for a few months, will result in it being unable to walk or operate properly, due to the lack of any non-random input during it's early critical periods for motor skills.

    Something else that's interesting and get's muddied over a lot, is that there are also "Sensitive periods" (SP), which are periods of increased experience dependant neural plasticity, synaptic plasticity (not the same thing!) and environmental sensitivity. In a nutshell, that means that the effects of experience on the brain are enhanced. This is a Quantitative Difference, as opposed to a qualitative one (CP), and the neural machinery involved is still malleable after the SP is "over". Still, the effects are quite noticeable, a prime example being the ability of babies to learn second+ languages (As opposed to adults), acquisition of social cues and behavioral norms by children and teenagers, etc'.

    Now, here's a cool bit - without going into detail overmuch (I'm aiming at research in the field), these days, we're getting an idea of the theoretical mechanisms maintaining plasticity or stability in the "mature" (as opposed to developing) brain, and we can manipulate the factors we've found already.
    As an example - The earlier example of Ambylopia? Induce it in a mouse, genetically modify said mouse so you can temporarily KO the molecular factors suspected to be involved in maintaining stability in the visual cortical... And the mice recovered vision :D. (This has obvious clinical applications, and immense theoretical implications in terms of altering adult, mammal brain stability)
    Some other cool examples is use of an anti-epileptic drug (Valproate) to reopen the CP in adults for learning perfect pitch (auditory system).
Some sources on the latter, cool stuff:
Lynx1, a Cholinergic Brake, Limits Plasticity in Adult Visual Cortex
Hirofumi Morishita, et al. Science
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3387538/ - OpenAccess link.

Valproate reopens critical-period learning of absolute pitch
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3848041/

Here's a rather nice review on the topic of critical and sensitive periods, and the recent work on brakes (vs pedals) on cortical plasticity:
https://dana.org/Cerebrum/2012/Re-openi ... velopment/

Or you could ask me :). (I'll be recording my next seminar where i'll be talking about it, but it might end up being in Hebrew :P)
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Re:

Post by Broomstick » 2014-05-20 09:40am

Fire Fly wrote:
Ace Pace wrote:Thats pretty damn awesome. One question though is whether any such expiriments are preformed on humans or is it simply too problematic (ethically, legally) to actually do any research there?
It can't be done in humans; the best you'll be able to do are non-invasive studies with imaging techniques or study in non-human primates.
Well, we can do some study on humans that have suffered various forms of physical insult or disability. If I recall, it's been found that in congenitally deaf children some of what would normally be the auditory area is taken over by the visual cortex or other systems. Certainly, people who lose their dominant hand can reprogram their remaining hand to do those same tasks although it requires considerable effort. These would pretty much be non-invasive testing, unless someone decides to donate their brain after death.
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Re: Re:

Post by The Grim Squeaker » 2014-05-20 02:03pm

Broomstick wrote:
Fire Fly wrote: It can't be done in humans; the best you'll be able to do are non-invasive studies with imaging techniques or study in non-human primates.
Well, we can do some study on humans that have suffered various forms of physical insult or disability. If I recall, it's been found that in congenitally deaf children some of what would normally be the auditory area is taken over by the visual cortex or other systems. Certainly, people who lose their dominant hand can reprogram their remaining hand to do those same tasks although it requires considerable effort. These would pretty much be non-invasive testing, unless someone decides to donate their brain after death.
This actually also happens in adults who suffer loss of one sensory modality or another.
(AKA - Blind people really do have better sensory acuity in other sensory modalities. And more grey matter devoted to those other senses).

1. Bavelier, D. & Neville, H. J. Cross-modal plasticity: where and how? Nat. Rev. Neurosci. 3, 443–52 (2002).
2. Bedny, M., Pascual-Leone, A., Dodell-Feder, D., Fedorenko, E. & Saxe, R. Language processing in the occipital cortex of congenitally blind adults. Proc. Natl. Acad. Sci. U. S. A. 108, 4429–34 (2011).
3. Collignon, O., Voss, P., Lassonde, M. & Lepore, F. Cross-modal plasticity for the spatial processing of sounds in visually deprived subjects. Exp. Brain Res. 192, 343–58 (2009).
4. Hugdahl, K. et al. Blind individuals show enhanced perceptual and attentional sensitivity for identification of speech sounds. Brain Res. 19, 28–32 (2004).
5. Lomber, S. G., Meredith, M. A. & Kral, A. Cross-modal plasticity in specific auditory cortices underlies visual compensations in the deaf. Nat. Neurosci. 13, 1421–7 (2010).
6. Merabet, L. B. & Pascual-Leone, A. Neural reorganization following sensory loss: the opportunity of change. Nat. Rev. Neurosci. 11, 44–52 (2010).
7. Noppeney, U. The effects of visual deprivation on functional and structural organization of the human brain. Neurosci. Biobehav. Rev. 31, 1169–80 (2007).
8. Osaki, Y. et al. Cortical processing of tactile language in a postlingually deaf-blind subject. Neuroreport 15, 287–291 (2004).
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