The Synaptogenesis Is the formation of synapses between the neurons of the nervous system . The Synapses Means the union 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 a single direction. So there is a neuron called"presynaptic"that is the one that sends messages, and a"postsynaptic"that 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 trillions of synapses exchanging data in the brain.
Synaptogenesis occurs continuously in our nervous system. As we learn and experience new experiences, new neural connections are forming in our brain. This occurs in all animals with brains, although it is especially pronounced in humans.
As for the brain , The bigger does not mean it is better. For example, Albert Einstein had a brain of a completely normal size. It has been deduced that intelligence is related to the number 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 external and internal stimuli it receives. For example, while you are reading this text it is possible that new brain connections will form if in a few days you keep remembering it.
Synaptogenesis in the Neurodevelopment
The first synapses can be observed over the fifth month of embryonic development. Specifically, synaptogenesis begins around eighteen weeks of gestation and continues to change throughout life.
During this period, synaptic redundancy occurs. This means that more connections are established in the account and are gradually being selectively eliminated over time. Thus, synaptic density decreases with age.
Surprisingly, researchers have found a second period of high synaptogenesis: adolescence. However, this growth is not as intense as that during intrauterine development.
Critical period
There is a fundamental critical period in synaptogenesis that is followed by a synaptic pruning. This means that neural connections that are not used or are unnecessary are removed. In that period, neurons compete with each other to create new, more efficient connections.
There seems to be 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 in this stage are determined by the genetics of the person. After this critical period, deleted connections can not be recovered in later life.
Thanks to the research, babies are known to learn any language before synaptic pruning begins. This is because their brains, full of synapses, are prepared to adapt to any environment.
That is why, at this moment, they can differentiate all the sounds of different languages without difficulties and are predisposed to learn them.
However, once exposed to the sounds of the mother tongue, they begin to become accustomed to them and to identify them much more quickly over time.
This is due to the process of neuronal pruning, maintaining 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 be more or less durable depending on how often 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 many times in our lives.
When a synapse is born, it has a lot of innervations. This is because new axons tend to innervate synapses that already exist, making them firmer.
However, when the synapse is maturing it differentiates and separates from the others. At the same time, the other connections between axons are retracted minus the mature connection. This process is called synaptic elimination.
Another sign of maturation is that the terminal button of the postsynaptic neuron increases in size, and small bridges of union between both are created.
Reactive synaptogenesis
Perhaps, by this point, you've already wondered what happens after brain damage that destroys some existing synapses.
As you know, the brain is constantly changing and has plasticity. That is why, after an injury, the 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 establish synapses properly. For example, if the patient is not receiving a 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 with neurodegenerative diseases.
In these diseases, among which are the Parkinson's and the Alzheimer's , There are a number of molecular alterations not yet fully known. These lead to the massive and progressive elimination of synapses, reflected in cognitive and motor deficits.
One of the alterations that have been found is in the Astrocytes , a kind of Glial cells Which intervene in synaptogenesis (among other processes).
It appears that autism also has abnormalities in synaptogenesis. It has been found that this neurobiological disorder is characterized by an imbalance between the number of excitatory and inhibitory synapses.
This is due to mutations in the genes that control this balance. This results in alterations in structural and functional synaptogenesis, as well as in synaptic plasticity. Apparently, this also occurs in epilepsy, the Rett syndrome , The one of Angelman And that of Fragile X (García, Dominguez and Pereira, 2012).
References
- García-Peñas, J., Domínguez-Carral, J., & Pereira-Bezanilla, E. (2012). Alterations of synaptogenesis in autism. Etiopathogenic and therapeutic implications. Journal of Neurology, 54 (Suppl 1), S41-50.
- Guillamón-Vivancos, T., Gómez-Pinedo, U., & Matías-Guiu, J. (2015). Astrocytes in neurodegenerative diseases (I): function and molecular characterization. Neurology, 30 (2), 119-129.
- Martínez, B., Rubiera, A. B., Calle, G., & Vedado, M. P. D. L. R. (2008). Some considerations about neuroplasticity and cerebrovascular disease. Geroinfo, 3 (2).
- Rosselli, M., Matute, E., & Ardila, A. (2010). Neuropsychology of child development. Mexico, Bogotá: Editorial The Modern Manual.