Long-term Empowerment: What It Is And How It Explains Learning
It is common sense that the more you study, the more information is retained in the brain. It is for this reason that, rather than studying all at once the day before an exam, it is recommended to dedicate half an hour a day to it during the two weeks before.
All this is already something obvious, however, although it is common sense, what we do not know so well is what its physiological explanation is. What changes occur in the brain so that we can retain information?
Well then, The biochemical process at the brain level that is behind learning and memory is called long-term potentiation and it is a very interesting aspect of our brain that we are going to learn about next.
Long-term empowerment is a process that occurs in the membrane of the neuron that explains how it is possible to establish learning and what its physiological bases are The process occurs when information is reviewed several times, causing the neuron to become sensitized and more reactive to lower action potentials, allowing it to more easily remember what has been learned.
The concept is quite complex, and before explaining it in more depth it is necessary to review its historical background in order to later look in more detail at how the process itself occurs.
Historical background
Years ago, scientists were searching for the exact place in the brain where brain functions occurred. Later, they discovered that different parts can participate in the same function It is known that various structures are involved in learning and memory: hippocampus, amygdala, brain and basal ganglia.
In 1970, an American scientist named Eric Kandel studied the sea slug Aplysia, in which he was able to discover some biochemical phenomena that occur in neurons while learning. It may seem surprising that a slug is related to the human brain, although it is clear that their brains are not the same, the slug being an invertebrate. However, despite the differences between the nervous systems of vertebrates and invertebrates, the brain chemistry of the neuron, their action potentials and neurotransmitters are the same
Before the studies in Aplysia, a scientist named Donald Hebb proposed, in 1949, a hypothesis to understand the change at the cellular level that occurs during learning. He suggested that when learning occurs a metabolic change occurs in neurons. However, it was not until 1973 when Terje Lømo, a Norwegian physiologist, studying the hippocampus of rats, discovered a phenomenon that was not expected: long-term potentiation, this neuronal metabolic change being suspected by Hebb.
The human brain has the ability to store information, either for brief periods of time, in short-term memory, or for life, in long-term memory. This can be verified, in a practical way, when we study for an exam. While we are studying, we activate several pathways inside our brain, pathways with which we manage to store, through repetition, the information that we have reviewed. The more the information is reviewed, the more it will be retained.
Long-term memory has been fundamentally associated with a structure whose shape resembles that of a seahorse: the hippocampus. This brain structure is located in the medial temporal lobe of both hemispheres, and is what is responsible for coordinating the storage of information and the retrieval of memories Research has focused attention on this part of the brain, when they have tried to study the learning process, especially its various structures: the dentate gyrus, CA1 and CA3.
The memorization process begins when information reaches the dentate gyrus from the entorhinal cortex The axons of the granule neurons project their axons to the cells of area CA3, which in turn project the information through the so-called Schaffer collaterals to the cells of field CA1 and, from there, through the subiculum, the information returns to the entorhinal cortex.
This whole process is long-term empowerment, which It is about the cellular and molecular process of memory This long-term potentiation involves the lasting improvement of signal transmission between two neurons after repeated stimulation. This process has been mostly studied in the synapses between Schaffer collaterals and neurons in the CA1 field.
Observing the synapses between CA3 and CA1 cells reveals multiple structures that are related to long-term potentiation. NMDA and AMPA receptors can be found in the postsynaptic neuron which are normally found together. These receptors are activated after the neurotransmitter fuses with the cell membrane and is released into the space between neurons.
The AMPA receptor is permeable to sodium ions, that is, it allows them to enter the interior of the neuron. The NMDA receptor is also permeable to sodium ions, but it is also permeable to calcium ions. NMDA receptors are blocked by a magnesium ion, which prevents sodium and calcium ions from entering the cell.
When an action potential travels along the presynaptic axon of the Schaffer collaterals, it occurs. the release of glutamate, a neurotransmitter which fuses with AMPA and NMDA receptors When this electrochemical stimulus is of low power, the amount of glutamate that is released is low.
The AMPA receptors open and a small amount of sodium enters the neuron, causing a small depolarization to occur, that is, the electrical charge of the neuron increases. Glutamate also binds to NMDA receptors, but no ion will be able to get past it because the magnesium ion continues to block it.
When the received signal is small, the postsynaptic response is not sufficient to achieve the output of the magnesium ion, so long-term potentiation does not occur. This is a situation that can occur, for example, when you have been studying for a very short time. A high frequency of action potentials have not been activated since so little has been studied, which has not induced this process of knowledge retention.
On the other hand, when there is a high frequency of action potentials, traveling through the Schaffer collateral axons, a greater amount of glutamate is released into the synaptic cleft This can be achieved if it is studied more, since a higher frequency of action potentials is encouraged. Glutamate will bind to AMPA receptors, causing a greater amount of sodium to enter the interior of the neuron thanks to the channel remaining open for longer.
That the more sodium inside the cell causes its depolarization to occur, managing to repel the magnesium ion from the NMDA receptor thanks to a process called electrostatic repulsion. At this point, the glutamate-activated NMDA receptor allows sodium and calcium to enter through its pore. NMDA receptors are called voltage- and ligand-dependent receptors because they require presynaptic and postsynaptic excitation for channel opening: fusion of the released presynaptic glutamate and depolarization of the postsynaptic cell.
Strengthening synapses
Long-term empowerment is a process that implies that the connection between two neurons is strengthened The introduction of calcium into the postsynaptic neuron acts as a second messenger, activating multiple intracellular processes. The increase in calcium leads to two processes involved in long-term potentiation: the early phase and the late phase.
During the early phase calcium fuses with its fusion proteins causing the insertion of new AMPA channels into the cell membrane of the synapse between field cells CA1 and CA3.
These new AMPA receptors were stored inside the neuron, and are only released thanks to the influx of calcium that comes from the NMDA receptor. Thanks to this, AMPA channels will be available in future synaptic connections. The changes induced during the early phase only last a few hours.
late phase
During the late phase, there is a greater entry of calcium, which causes genetic transcription factors to be activated that cause new proteins to be synthesized. Some of these proteins will end up being new AMPA receptors, which will be inserted into the neuronal membrane.
In addition, there is an increase in the synthesis of growth factor proteins, which lead to the growth of new synapses and are the basis of synaptic plasticity. So, in this way, the brain changes as it lights up.
These synapses are formed between CA1 and CA3 neurons, allowing for a stronger connection. The late phase changes are longer lasting, ranging from 24 hours to a lifetime.
It should be noted that long-term potentiation is not a mechanism, but rather an increase in activity between two neurons, which results in an increase in the AMPA channels of the neurons that will allow, even with low frequencies of action potentials, creates cellular depolarization when, before, it was necessary for a high frequency of potentials to occur to achieve this objective.
This whole process is the foundation of memory. However, it is worth noting that The hippocampus is not the only region where long-term potentiation occurs Memory processing occurs in many other brain regions, including the cerebral cortex. Be that as it may, one must be clear about the fact that the more one studies, the more pathways are activated throughout the brain, making learning become more consolidated.
