Neuroplasticity part 1 - Introduction to neuroplasticity:

Throughout our lives we are shaped by our experiences. They not only change our behaviour but even how we think.These psychological changes are the result of corresponding physical changes in the connections between the neurones in our brains.

We have a view that the structure of our brain is fixed, but the function of our brain is to interpret the environment, discover relationships and change our behaviour accordingly. Our brain is not a static organ and indeed to function properly it needs to be dynamic and changing on every level.

This changing and shaping of the connections in our brain is known as neuroplasticity.

Hebbian plasticity:

The first person to notice this “plastic” nature of the brain was the Canadian psychologist Donald Hebb.

In his book the organization of behaviour, he wrote his now classic Hebb’s postulate:

“When an axon of cell A is near enough to excite a cell B and repeatedly or persistently takes part in firing it, some growth process of metabolic change takes place in one or both cells such that’s As efficiency as one of the cell firing B in increased”

Simply put;

When two neurones fire at the same time, the connections between them are strengthened, and thus they become more likely to fire again together in the future.

When two neurones repeatedly fire in an uncoordinated manner, the connections between them weaken, and they are more likely to act independently in the future.

This can be simplified to the mantra:

• ·         Cells that fire together, wire together.
• ·         Cells that fire apart, wire apart.

These plastic mechanisms form the basis of the brains ability to change in the face of the environment, to learn and remember.

Plasticity, memory and learning:

But how do these plastic changes form the basis of learning and memory?

The type of learning plasticity has been applied to most is classical conditioning.

The most famous example of classical conditioning is Pavlov’s dogs,

a stimulus (food) which produced a response (salivation), was paired with a stimulus that did not produce a response (bell.)

After multiple exposures, the bell produced the same response (salivation) even without the presence of the original stimulus (the food)

the similarities with Hebb’s postulate are easily seen.

The neurones responsible for the bell and the neurones responsible for the salivation were repeatedly activated at the same time, this strengthened the synaptic connections between them, and so in the future they were activated together.

When we learn something, a set of neurones are triggered and become connected. This now connected “assembly” of cells persists, and if this set of neurones is triggered again, we will re-experience the event as a memory.

The theoretical memory trace In the brain is known as an Engram

The relationship between cell assemblies and memory was initially investigated by Karl Lashley.

He taught a rat to complete a maze, then destroyed a different part of the cortex each time, and would see which area affected the maze memory.

                                                             

The only relationship he found was that the number of errors made was directly proportion to the amount of cortex destroyed.

	Lashley concluded that memory is equally distributed in all cortical areas, through these interconnected cell assemblies*.

Storing information in assemblies like this can also explain another phenomenon of memory, how only a partial cue can trigger the reactivation of a whole memory, for example how a small detail, such as a familiar smell can cause to us relive a detailed memory.

Activation of a single part of the assembly will reverberate through all its connections, activating other cells encoded at the same time.

                                                                                                                                                                         

 Now can see very basically how the brains ability to change itself and alter its connections, enable it to learn meaningful relationships and store this learnt knowledge as memories, in the form of cell assemblies, which may be activated again upon presentation of only part of a familiar experience.

Sources:

Mu-ming Poo Part 1: The Cellular Basis of Learning and Memory. http://www.ibioseminars.org

Hebb, D.O. (1949). The organization of behaviour. New York: Wiley & Sons

The Brain that changes itself: Dr Norman Doidge,

The method of pawlow in animal psychology. Robert M. Yerkes and Sergius Morgulis (1909).Harvard University. First published in The Psychological Bulletin, 6, 257-273.

The neurobiology of consolidations, or, how stable is the engram? Dudai Y. Annu Rev. Psychol. 2004;55:51-86.

Studies of cerebral function in learning IX. Mass action in relation to the number of elements in the problem to be learned^† Lashely and wiley 1933. The Journal of Comparative Neurology. Volume 57, Issue 1, pages 3–55, February 1933

*”we now know that Lashely’s experiment did not distinguish between memory or motor areas, and so the rats impairment in the maze may not be due to memory impairment but instead the impairment of its motor functions. The current view is that memory is indeed distributed by not, but not equally. Some areas such as the hippocampus paly a particularly crucial role, which we will discuss later.”