The biological processes that underlie neuroplasticity take place at both the microscopic and macroscopic levels. Microscopic mechanisms include neurogenesis, synaptic activity modifications, reactivation of latent synaptic networks, and modulation of neural circuits mediated by glia and an extracellular matrix. During the early stages of development, the proliferation and differentiation of neurons and their structures (e.g., dendrites and axons), as well as their connections through synapses, take place [
14]. Afterward, because of sense stimulation and experience, these networks are molded through apoptosis and the modification or regression of synaptic connections [
15,
16]. These structural changes may also take place after a brain injury, showing renovation in particular dendrites [
17]. There is also evidence concerning the role of neurotrophins (NTs) in neural plasticity, mediating the differentiation and survival of neurons in synaptic transmission and reshaping [
18,
19]. In addition to neurogenesis, synaptic plasticity plays an important role in the brain’s reorganization. It refers to the modulation of synaptic efficacy due to repetitive nerve impulses. Thus, this process is based on changing the stimulation from a presynaptic to postsynaptic cell, providing an increase or decrease in synaptic efficacy, named long-term potentiation (LTP) and long-term depression (LTD), respectively [
2,
5,
20,
21]. LTP originates from rapid presynaptic depolarization of the synapses, which activates NMDA-type glutamate receptors in the postsynaptic membrane, causing a rise in intracellular Ca
++ levels. This induces the expression of AMPA-type glutamate receptors in the postsynaptic membrane, leading to an increase in synaptic strength. It also causes the release of brain-derived neuronal growth factor (BDNF) in neurons, which enhances LTP and enlarges the dendrites ([
5,
22] “AMPARs and synaptic plasticity: The last 25 years”). On the contrary, LTD comes from slow repetitive stimulation of the synapses, which causes a migration of AMPA receptors in the cytoplasm [
20]. While LTP has a key role in learning and memorization, as seen in the hippocampus, both LTP and LTD seem to mediate the reorganization of neural networks in the sensory motor cortex [
23]. In a review article, Sheperd et al. described how
ARC gene expression is involved in the regulation of synaptic plasticity. In fact, it seems to control the neural output of excitatory neurons by facilitating LTD and by modulating the expression of AMPA glutamate receptors [
24,
25]. In a work by Pfeiffer, B. and Huber, K., it is explained how, in order to maintain LTP and LTD as functional synaptic changes in the cortical areas, it seems that local or dendritic specific protein synthesis is required [
26]. Another kind of synaptic plasticity is represented by the conversion of silent synapses in active connections. The organization of cortical networks in functional areas is granted by the activity of inhibitor GABA interneurons, which stop the horizontal connections between different areas. Events such as sensory deprivation or learning may interrupt this kind of control, unleashing these latent connections and creating a sort of short-term plasticity [
27,
28]. A synapse’s activity can also be directly influenced by neuroglia. This wide network, through the production of neurotransmitters and extracellular mediators, has the potential to improve synaptic transmission [
29,
30]. Moreover, glial cells can also communicate with each other by using gap junctions and intracellular messengers [
31] to coordinate the activity of neural networks. Control of the neuronal activity is also accomplished by the extracellular matrix [
32].