SYNAPTOGENESIS: DEVELOPMENT, MATURATION AND DISEASES - GEOGRAFÍA - 2025

The synaptogenesis is the formation of synapses between neurons of the nervous system. A synapse is a junction or contact between two neurons, which allows them to communicate with each other, contributing to our cognitive processes.

The exchange of information between two neurons is usually in one direction. So there is a neuron called "presynaptic" which is what sends messages, and a "postsynaptic" which is the one that receives them.

Although synaptogenesis occurs throughout the life of a human being, there are stages where it occurs much more rapidly than in others. This process maintains several trillion synapses exchanging data in the brain.

Synaptogenesis occurs continuously in our nervous system. As we learn and live new experiences, new neural connections are formed in our brain. This occurs in all brained animals, although it is especially pronounced in humans.

As for the brain, bigger doesn't mean better. For example, Albert Einstein had a brain of a completely normal size. So it has been deduced that intelligence is related to the amount of connections between brain cells rather than the number of neurons.

It is true that genetics play a fundamental role in the creation of synapses. However, the maintenance of the synapse is determined, to a greater extent, by the environment. This is due to a phenomenon called brain plasticity.

This means that the brain has the ability to change according to the external and internal stimuli it receives. For example, while you are reading this text, new brain connections may form if you keep remembering it in a few days.

Synaptogenesis in neurodevelopment

The first synapses can be observed around the fifth month of embryonic development. Specifically, synaptogenesis begins around eighteen weeks of gestation and continues to change throughout life.

During this period, a synaptic redundancy occurs. This means that more connections are established on the account and little by little they are selectively eliminated over time. Thus, the synaptic density decreases with age.

Surprisingly, researchers have found a second period of elevated synaptogenesis: adolescence. However, this growth is not as intense as that which occurs during intrauterine development.

Critical period

Neuron

There is a critical critical period in synaptogenesis that is followed by synaptic pruning. This means that unused or unnecessary neural connections are removed. During this period, neurons compete with each other to create new, more efficient connections.

It appears that there is an inverse relationship between synaptic density and cognitive abilities. In this way, our cognitive functions are refined and become more efficient as the number of synapses is reduced.

The number of synapses that originate at this stage are determined by the individual's genetics. After this critical period, deleted connections cannot be recovered in later life.

Thanks to research, it is known that babies can learn any language before synaptic pruning begins. This is because their brains, full of synapses, are prepared to adapt to any environment.

Therefore, at this time, they can differentiate all the sounds of different languages ​​without difficulty and are predisposed to learn them.

However, once exposed to the sounds of the mother tongue, they begin to get used to them and to identify them much more quickly over time.

This is due to the neural pruning process, keeping the synapses that have been most used (those that support, for example, the sounds of the mother tongue) and discarding those that are not considered useful.

Synaptic maturation

Once a synapse is established, it can last more or less depending on how many times we repeat a behavior.

For example, remembering our name would mean very well established synapses, which are almost impossible to break, since we have evoked it many times in our lives.

When a synapse is born, it has a large number of innervations. This occurs because new axons tend to innervate existing synapses, making them firmer.

However, as the synapse matures it differentiates and separates from the others. At the same time, the other connections between axons retract less than the mature connection. This process is called synaptic clearance.

Another sign of maturation is that the terminal button of the postsynaptic neuron increases in size, and small bridges are created between them.

Reactive synaptogenesis

Perhaps, at this point, you have already wondered what happens after brain damage that destroys some existing synapses.

As you know, the brain is constantly changing and has plasticity. Therefore, after injury, so-called reactive synaptogenesis occurs.

It consists of new axons that sprout from an undamaged axon, growing into an empty synaptic site. This process is guided by proteins such as cadherins, laminin, and integrin. (Dedeu, Rodríguez, Brown, Barbie, 2008).

However, it is important to note that they do not always grow or synapse properly. For example, if the patient is not receiving correct treatment after brain injury, this synaptogenesis may be maladaptive.

Diseases that influence synaptogenesis

The alteration of synaptogenesis has been related to several conditions, mainly neurodegenerative diseases.

In these diseases, among which are Parkinson's and Alzheimer's, there are a series of molecular alterations that are not yet fully understood. These lead to the massive and progressive elimination of synapses, reflecting in cognitive and motor deficits.

One of the alterations that have been found is in astrocytes, a type of glial cells that are involved in synaptogenesis (among other processes).

It appears that in autism there are also abnormalities in synaptogenesis. This neurobiological disorder has been found to be characterized by an imbalance between the number of excitatory and inhibitory synapses.

This is due to mutations in the genes that control this balance. What results in alterations in structural and functional synaptogenesis, as well as in synaptic plasticity. This also appears to occur in epilepsy, Rett syndrome, Angelman syndrome, and Fragile X syndrome.

References

1. García-Peñas, J., Domínguez-Carral, J., & Pereira-Bezanilla, E. (2012). Synaptogenesis disorders in autism. Aetiopathogenic and therapeutic implications. Revista de Neurología, 54 (Suppl 1), S41-50.
2. Guillamón-Vivancos, T., Gómez-Pinedo, U., & Matías-Guiu, J. (2015). Astrocytes in neurodegenerative diseases (I): function and molecular characterization. Neurology, 30 (2), 119-129.
3. Martínez, B., Rubiera, AB, Calle, G., & Vedado, MPDLR (2008). Some considerations on neuroplasticity and cerebrovascular disease. Geroinfo, 3 (2).
4. Rosselli, M., Matute, E., & Ardila, A. (2010). Neuropsychology of child development. Mexico, Bogotá: Editorial El Manual Moderno.