Open to criticism - Is synaptic plasticity the neural basis of learning and memory?

Is synaptic plasticity the neural basis of learning and memory?

Scientifically, it is well known that learning and memory must occur within the brain as it is the primary organ that allows us to function as human beings. However the process by which this occurs is currently unknown, but several cases have been studied towards a conclusion. The central hypothesize used by scientists today to overcome this mystery is the occurrence of long term potentiation- one type of synaptic plasticity. In neuroscience, synaptic plasticity is the occurring change of the strength of a synapse through the altering of stimulation by the presynaptic neuron. In this essay I will be discussing the properties of LTP followed by evidence to suggest whether it is or isn’t the neural basis of learning and memory.

Synaptic plasticity, commonly referred as the neural basis of knowledge and memory, occurs in the space between two or more neurons called the synapse. One type of this is called long term potentiation, or LTP, which is ultimately believed to enhance synaptic transmission:a change in the strength of connection between two neurons. During this process, the neurons use electrochemical signals to communicate with each other. When the presynaptic neuron is stimulated by an action potential, it triggers the release of calcium ions which are used by the vesicles to bind with the membrane. This causes the release of neurotransmitters across the synapse towards the receptors in the postsynaptic neuron. As a result, neurotransmitter-gated
channels open to allow sodium and calcium ions to flow into the postsynaptic neuron (calcium only enters through NMDA receptors during synaptic plasticity). This occurs because the action potential reaches threshold of approximately -50m. Once the sodium ions enter the postsynaptic neuron, another action potential is triggered within it if the threshold is reached in the PSP (postsynaptic potential). In addition, the interior of the postsynaptic membrane has a different charge to the exterior. This difference is called the postsynaptic potential and is affected by the number of ions that flow into the postsynaptic neuron. Due to this, we are able to measure the strength of the synapse as we can determine how much the postsynaptic neuron’s potential changes as a result of presynaptic stimulation. Ultimately, after a long period of time the synapse strengthens due to repetition of the process ( this involves the use of more neurotransmitters and calcium ions).



Source:http://www.expertsmind.com/topic/neuroscience
/long-term-potentiation-93811.asp

There are two main alterations that are believed to have a lasting effect on the process of long term potentiation. These factors involve: the change of rate at which glutamate is released (and amount); and the amount of AMPA receptors located on the postsynaptic membrane. As a result, if there is an increase of both AMPA receptors as well as glutamate, then the postsynaptic potential’s gradient will become steeper due to each presynaptic potential opening more channels to allow more sodium to flow in. To have more AMPA receptors, the process of long term potentiation has to occur between two (or more) pre-synaptic neurons, and one postsynaptic neuron. This is because there are two types of receptors that are present on the postsynaptic membrane; AMPA and NMDA receptors. NMDA receptor may only open once the action potential has reached threshold within the postsynaptic neuron, and when magnesium is repelled out of its channel as a result of positively charged ions being present (such as sodium). Once opened, more sodium ions are able to enter the postsynaptic neuron, as well as calcium. These calcium ions bind to signalling proteins called calmodulin causing them to primarily insert more AMPA receptors into the postsynaptic membrane. As a result, this allows even more sodium to flow into the postsynaptic neuron which increases the chances for the PSP (postsynaptic potential) to reach threshold. This is process is also part of Pavlovian Conditioning.



Pavlovian learning (named after Ivan Pavlov) occurs when an organism understands the relationship between a conditioned and unconditioned stimulus so that it may produce the same response to either one.This is related to long term potentiation as both share similar properties of: being specific as both may only occur when the requirements are met (LTP: increase of calcium for AMPA receptors to be produced ;Pavlovian learning:only a bell produces the same response) ; being cooperative as they need the co-presentation of both stimulations (LTP: the firing of both neurons; Pavlovian learning: the presentation of food and the bell during conditioning); and having temporal contiguity as they may only occur within small time-window (LTP: both neurones must fire at the same time; Pavlovian learning: the conditioned and unconditioned stimulus must be present during the same time).

An example of Pavlovian Conditioning is when a dog produces the same response of salivation to the food (unconditioned stimulus) as well as the bell (conditioned stimulus). This may only occur after months of repetition (the same as for long term potentiation) until the dog learns that the sound of the bell represents the arrival of food. Training includes having the dog both see and hear the stimuli so that the presynaptic neuron of the neutral stimulus (sound of a bell before conditioning) may cause the trigger of an action potential by itself within the postsynaptic neuron (cause of the salivation) . This requires the insertion of AMPA receptors in the area of NMDA receptors which follows the process of long term potentiation. Furthermore, an example would show that a neuron which fires upon the sound of a bell is not sufficient enough to cause the salivation response as the PSP would still be sub-threshold. However, when both the presynaptic neurons of the bell and food have been fired, then the strength of the synapse increases as the PSP does reach threshold for salivation to be caused. As a result, the strength of the synapse will reach the point at which either the bell or the food alone will be sufficient enough to cause the response. Ultimately the similarities of LTP and Pavlovian learning lead to suggest that synaptic plasticity may be the neural basis for learning, as well as memory (seeing that the dog would remember this relationship for months).



Source: http://animals.howstuffworks.com/pets/dog-training1.htm

Even though Pavlovian conditioning and long term potentiation are similar, the evidence is somewhat weak as it is not enough to prove that LTP is the initial cause of this simple form of learning. To to do so we must consider the general two types of evidence which are sufficiency and necessity. Sufficiency would be difficult to demonstrate as there are billions of neurons in the brain thus we would not be able to determine what the effects would be if LTP would be induced within a random synapse. Necessity on the other hand is easier to demonstrate as we already know that if NMDA receptors were to be blocked (or calcium to be reduced), thus declining the entrance of calcium into the postsynaptic neuron, then LTP will not be induced properly.

Due to this, it is clear that following the induction of APV in the synapse, long term potentiation will be prevented as this cause the blockading of NMDA receptors thus there will be no increase of the postsynaptic potential. Richard Morris carried out this experiment wherein he and his colleagues applied APV to a rat’s brain who later was unable to learn the location of the platform in a water maze. This was also repeated without the use of APV which showed results of the rat swimming around the location of the platform. As a result, this shows that long term potentiation does cause learning as without it an organism (a rat in this case) will not be able to recognise information to an extent. Malenka carried out a similar experiment wherein he showed that adding a calcium chelator to the brain (not within an animal) will prevent LTP if done so after tetanic stimulation.

We’ve seen how LTP could be the neural basis for learning and memory, but what evidence is there to show that it may not be. Firstly we must consider the fact that Pavlovian conditioning can occur even with greater time gaps between the conditioned and unconditioned stimulus. An example would be becoming ill after eating some food, thus learning to dislike it. Whereas long term potentiation can only arise within short-time windows of about 100ms. Therefore how can pavlovian conditioning occur if LTP arises at a much earlier period of time. Secondly, there are some chemicals apart from APV (such as protein kinase C) which can block long term potentiation, however learning still takes place.

Theoretically, if long term potentiation is not the cause of learning and memory, then what is it doing? Currently up to this day, LTP has been found within every single synapse that has been studied on, therefore what purpose may it have that it is present within such an important part of our brain. Additionally, we must also remember that LTP is only one form of synaptic plasticity, therefore we cannot consider it as the only possible cause of learning and memory. Even though LTP is good at explaining how pavlovian learning works, it is harder for it to explain how more complex learning occurs such as motor learning.

Throughout this essay, we’ve discussed and outlined a balanced argument for whether synaptic plasticity is in fact the neural basis for learning. However, we have only considered a few of many forms of learning and memory to an extent where we cannot fully agree on whether it is or isn’t. Currently, I am more willing to say that it is as most of the evidence points in that favour. On the other hand, there is still plenty of evidence which continue to counter each other, thus making a conclusion less of a possibility. Ultimately, we know too little about the brain at this point in time to confidently say that it is or isn’t. And so with time, will come an answer that we all can agree on in the future.

By Dionyzas Treigys
Age: 16