**3. Neuroplasticity**

#### **3.1 An approach from neuroembryology**

To fully understand neuroplasticity, it is first necessary to classify and define what this concept stands for. Several authors have tried to state a formal definition,

#### *Neurophysiology Involved in Neuroplasticity: Mechanisms of Forgetting DOI: http://dx.doi.org/10.5772/intechopen.105129*

yet many of them have not taken into consideration this phenomenon over time. Neuroplasticity is a complex process that starts in the embryo neurogenesis, beginning with neurulation. It is important to state that the closure of the neural tube happens between the 21st and 25th day [3]. From the formation of the neural tube until the moment in which the fetus has a complete morphological nervous system many molecular signals initiate and finish the growth, connectivity, and cellular differentiation within the brain and the rest of the nervous system. Between the 8th week of pregnancy (time by which every human system is formed) to the moment of labor, the nervous system shifts drastically [4].

#### **3.2 The notch pathway and neuroplasticity**

One of the most important mechanisms of these changes is the Notch differentiation which is a gene-mediated regulatory cascade also known as the "notch signaling pathway". Its importance comes from its direct participation in cell proliferation and fate, so as differentiation and apoptotic mechanisms. This process assures the development and distinction of the nervous system from small animals (*i.e., Drosophila melanogaster*) to humans [5, 6].

Although this process elucidates how neuroblasts tend to differentiate into neurons and both glial cells, it should be said that the whole process is more complex than the intervention between the "Hes family (1, 5 & 6)", RBPJ and the ligands with Jagged and DII [7]. What can be said is that an incorrect step in the process might change future physiological functions within the nervous system, opening the possibility of mental illnesses and congenital neurological diseases which are not going to be described in this manuscript. Information regarding the topic has been published, but the reality is that studies just explain the correlation between multiple genes, transcripts, and proteins that take part in the complex process of neurological plasticity [8].

Also, epigenetic factors can alter the expression of this mechanism that takes place in embryogenesis and after-birth processes. Lasky states that memory and learning are two of the most important and multifactorial processes that involve a relationship with Notch, so as diverse pathologies that may arise from this process in postnatal development [9]. This evidence has also been restated a few years ago by Engler, adding the participation of NOTCH1 and NOTCH2 in this phenomenon, as well as adding a description of how all these factors take place in adults [10].

#### **3.3 Fresh perspectives regarding neuroplasticity**

The reality is that younger individuals have a better capacity than older ones to form neuronal connections, learn and perform new tasks, due to the capacity of younger neurons to arborize and form new circuits [11]. Adult neurogenesis, and thus neuroplasticity, is possible to occur in the hippocampus. This theory has been deeply discussed, but the reality is that more research and more substantial medical evidence should be published in order to get to a consensus [12]. Despite age, individuals that make exercise tend to have an increase in neurotrophic factors (*i.e.,* Brain-Derived Neurotrophic Factor, Nerve Growth Factor, and Glial Cell line-derived Factor) that brings a more efficient functionality in comparison with those who do not exercise [13]. The relationship between oxytocin and the increase of pro-social behaviors, neuronal excitability, and plasticity has been described by Froemke [14]. It is important to acknowledge that the research made by this group determined that mammals

use oxytocinergic modulation in the process of maternal care and social bonding. It is a prolific contribution to the field because of the hormonal and neurological modulation involved in physiological and pathophysiological processes.
