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Nelly Khaselev's picture
Is our Brain made out of Plastic?

            Since the day you were born, your brain and the nervous system has not stopped changing and adjusting. This constant changing and adjusting, is what most scientist claim to be the cause or the effect of learning. The cause of learning and the effect of learning are quite two different elements scientists have been studied and are thoroughly debated. Learning is one of the most enticing capabilities of our brain. How we learn to walk and talk? How we learn to drive a car? How we form memories? These are all questions that the scientists pose themselves to discover more about the human brain, the nervous system and its connection to the idea of learning. There are several theories and explanations for these questions; the most widespread is the idea of brain plasticity and synaptic plasticity. What does this actually mean? According to most extensive data, there are two kinds of modifications that occur with learning, (weather these modifications are the cause of or the effect of learning is for yet another time). The first is an increase in the number of synapses between neurons; and the second is a change in the internal structure of the neuron- the synapses itself is changed.
Brain plasticity or neuroplasticity, is the ability of your brain to reorganize the architecture of its neurons and the neurons of the nervous system. The architecture of the nervous system is what distinguishes me from you, and you from every other person on this planet.  From the surface, the brain of every human looks very similar but then again every person will react differently in the same situations. If you look a little closer at the brain, you will see a different pattern of neurons and different synaptic connections; the architecture accounts for these different responses in every person and even in animals. The architecture is always changing as an effect of the person’s environment; forming, erasing (pruning) and reforming different patterns of synapses between neurons. In fact, at birth each neuron in the cerebral cortex has about 2,500 synapses. By the time the baby is two or three years old there are about 15,000 synapses per neuron. This is about two times that in an average human – this is due to pruning (the body’s way of getting rid of weak connections between neurons).
          An amazing example of the capability of brain plasticity can seen in my people who over come brain injury due to harsh impact to the brain (e.g. car accident) or a disease such as Huntington’s disease, Alzheimer's Disease, and others. Many of these diseases have no cure and people who suffer from them lose control of their own bodies. Fortunately, with more research someday more people will turn out to be like Judy. Judy is a young girl who suffered from Rasmussen syndrome – a brain degenerative syndrome that disrupts the electrical activity that makes the brains work. Rasmussen's syndrome is associated with slowly progressive neurologic deterioration and seizures. Judy at age three had seizures that could not be controlled from medicine. Doctors found that all her seizers were coming from her right hemisphere. The solution – Hemispherectomy; the removal of almost all of one hemisphere of the brain. It is simiply amazing how half a young girls brain could be removed and as little as ten days later, she walked out of the hospital. Brain placticity allowed for Judy’s brain to reform neural connections that controlled her body. To better understand the nature of such diseases that affect learning and forming memories, researches are looking deeper into brain placticy and have discovered the second modification of the nervous system that comes with learning.
         The brain is plastic throughout life - it is constantly changing. The ability to learn and form memories, things that we take so much for granted, comes about because of the ability of neurons to change the way in which they communicate with each other - that is, through synaptic plasticity – the second modification that comes with learning. To better understand synaptic plasticity, one would first need to understand what synapses are. Synapses are a way two neurons communicate via exchange of information. The synapse consists of the two neurons, one of which is sending information to the other. The sending neuron is known as the pre-synaptic neuron (i.e. before the synapse) while the receiving neuron is known as the post-synaptic neuron (i.e. after the synapse). Now, although the flow of information around the brain is achieved by electrical activity, communication between neurons is a chemical process.
        Some current research is being conducted to explain synaptic plasticity but it is currently believed that the post-synaptic response to the release of neurotransmitter (the message or signal) is not necessarily always the same. A lot of research is investigating how synaptic strength can be increased and decrease for different period of time. Long-term potentiation and Long-term Depression are two key concepts that have a strongly correlated connection with forming and storing memories.
          Long-term potentiation is constant stimulation of a connection between two neurons enhancing that specific pathway. It was discovered in the early 1970's in a region of the brain called the dentate gyrus, part of the hippocampal formation. In the most well understood form of LTP, enhanced communication is predominantly carried out by improving the postsynaptic cell's sensitivity to signals received from the presynaptic cell. One generally studied forms of LTP is known as NMDA receptor-dependent LTP. This form of LTP requires the activation of NMDA receptors, allowing an influx of calcium ions into the post-synaptic cell. NMDA receptor is a glutamate receptor (a simple ion channel receptor) that is named after the specific kind of chemical it interacts with. These receptors are permeable to sodium ions and thus generate depolarization waves – this is how information is transferred from one neuron to another. The influx of calcium is likely to be the result of a modification of the receptors, such as phosphorylation. A second mechanism by which NMDA receptor-dependent LTP may be expressed is from an increased number of AMPA receptors (another glutamate receptor that interacts with a different chemical) expressed on the post-synaptic cell surface.
           Research on this topic is extensive and very interesting. In general the way a pathway between two neurons is strengthened by an increase in a certain type of receptors and their sensitivity to a specific signal – according to one hypothesis. This is important to investigate because LTP and long-term memory are rapidly induced, each depends upon the synthesis of new proteins each has properties of associativity, and each can potentially last for many months. LTP may thus account for many types of learning, from the relatively simple classical conditioning present in all animals, to the more complex, higher-level cognition observed in humans.
         Long-term Depression is the weakening of a pathway between two neurons. One hypothesis suggests that the synaptic strength between a pre-synaptic neuron and a post-synaptic neuron is decreases by a continous low frequency stimuli. Another suggest that LTD is not due to decrease in current flow through receptors but instead the actual decrease of recpetors. The number of recepotros on the post-synaptic neuron can be reduced to the point where it no long responds to stimulation at all. This neurons has been “silenced.”
          Synaptic plasticity is the capability of synapses to change. The way a synapse changes depends on its previous history, the type of stimulation it recieves and its environment. A specific synapses can undergo either LTP or LTD, or both at different times throughout a person’s life. This is what scientist call bi-directionally modifiable synapses. The increase and decrease in synaptic strength can be seen in use in everyday actions. For instance, the visual recognition memory that resides in a region of the brain known as the peripheral cortex. In your brain, there are certain neurons that distinguish new objects from recognizable objects. The electrical activity of these neurons can be measured when different stimuli are present. It has been recorded that when you see a flower or any other familiar stimulus, less electrical activity flows through your brain then when you see something for the first time.
          The mechanisms of learning and memory are at the essence of how the brain works. These mechanisms are being investigated as we speak and new discoveries are being unfolded more and more. Brain plasticity and synaptic plasticity are only two possible stories to explain how our body learns out of the many possibilities. It is our inevitable curiosity that enables us to explore and get a less wrong understanding of our brain, the nervous system, and how we learn and form memories.

Works Cited
1. Brain Plasticity. 2007. Discovery Channel. 8 Apr. 2008 <>.
2. "Brain Plasticity." Venderbilt Kenndy Center. 8 Apr. 2008 <>.
3. "Central Nervous System Overview." Brain Connection. Oct. 2006. 8 Apr. 2008 <>.
4. Cooke, S F. "Plasticity in the Human Central Nervous System." Brain. May 2006. 8 Apr. 2008 <>.
5. "EpilepsyAction." 8 Apr. 2008 <>.
6. "How We Learn and Remember?" Brain Sciences. Nov. 2003. Brown University. 8 Apr. 2008 <>.
7. Lampsa, K P. "NMDA Receptor-Dependent Long-Term Potentiation." Ionchannels. 8 Apr. 2008 <>.
8. "Mechanisms of Synaptic Plasticity." Medical Research Council. 8 Apr. 2008 <>.


Paul Grobstein's picture

Brain "plasticity"

Its interesting that five or six decades ago, everyone assumed that the brain was continually shaped by experience, and that today we refer to "plasticity" as if its unexpected. I wonder why that is, and to what degree existing evidence on shaping by experience gets us closer to understanding memory or farther from it?