Brain Plasticity and learning

It is known that during development the architecture of brain associative and progressive connections are susceptible to modifications from the experience, however these changes become be apparently stationed in adulthood. Eventually, progressive connections also seem to lose plasticity while the synapses of associative connections remain one susceptibility for experience-dependent changes. The persistent adaptability of reciprocal connections is probably the key to the acquisition of skills that are generated due to patterns perceptual and engines throughout the life (Aguilar 2003; Díaz-Arribas, Pardo-Hervas, Tabares-Lavado, Rios-lago, Maestú, 2006). 

Yo-Yo Ma

At this sense, it will be the individual and surrounding external influences which decide in the end, what should be the lattice of synaptic networks that are formed. Thus for example, in string musicians, the area of the cortex which governs the fingering hand is greater than the hand that does not have so much execution; fingers most used  will have more cortex space. Another example of connections that can be developed is in the people who read Braille, whom visual cortex is activated when they felt the prominences of the writing with their fingers (Aguilar, 2005).

This is a possible explanation about why some behaviors should be developed early as swimming, walking or the speech, but once the adjustments have been made and neural trimming is obvious, what do we have?. Some authors explains of the functional maturity that occurs when surplus neuronal connections have been removed and plasticity begins to decline, the process depends on the survival of the more suitable connections, thus the so-called critical period of development ends when the neuronal removal process has come to the point is that only a few synapsis, if some remain, thay might still have competitive interaction.

However, it is not only environmental stimulation which can cause long-lasting modifications in neurodevelopment. An example of this can be found with stimulation such as tactile stimulation, postnatal, maintained in soft and permanent manner for some time after the birth (consistent touch manipulation) exerts beneficial effects in the form of a less emotional reactivity, for example is less likely to stress, greater learning ability in emotional situations. While that when stimulation is inconsistent because you drill them touch have been irregular in form and frequency, children have greater emotional reactivity and see reduced its capacity for some learning.

This could mean  that environment is able to modify the function and brain structure, in such a way that the experience has consequences at different levels of integration more or less enduring. This is especially true during the early stages of life in which the brain development in which experience has one greater importance, if possible, since it not only facilitates patterns, but it should be noted that the modification of a function is not always accompanied by modification of the structure, and this should have it present especially when the brain is subjected to incisive and constant disturbances that impede the expression of adaptive processes in all fullness (Flores, 2005).

So it has been speculated that rapid learning of infants, especially during critical periods, reflects the exploitation of the large number of synapses available at that time, some of which not be connected soon will be removed or pruned. Being so, when surplus cells have been removed and the number of neurons that innervate is adjusted, then the flexibility and plasticity of this early phase of life seems to decline (Patchev, Rodrigues, Sousa, Spengler and Almeida, 2014).

 

           Even though there are several examples reported on the changes of environment on cognitive development, the study on environmental enrichment is one that most have been reproduced and applied to the teaching and learning models in particular. This model, applied to animals, usually rodents, which were put cage larger than usual, and with the largest number of inhabitants per cage. The cages are placed toys of forms and various colours that are exchanging systematically; stairs, casters are included and there are difficulties in access to food that also varies in texture and flavor.

A classical study exlained that animals that have been subjected to this type of stimulation during various time periods (usually 1 or 2 months after weaning) presented substantial synaptic differences compared to peers who live in standard conditions, in this sense, is the first to better perform tests which require a complex learning, are more proficient in tests assessing memory space viso and short-term memory, and may even show late signs of aging. These results of a cognitive nature are accompanied by neuroanatomical changes, such as the increase of thickness of the cerebral cortex, the increase in the number of dendritic spines and the increase in the number and size of synapses, as well as increasing the process of neurogenesis. 

At the neurochemical level, also shown an increase in the expression of some genes that have to do with neural development, and changes in the operation of the signalling pathways intra-neuronal that are activated in response to different neurochemicals stimuli. By what the moral of the whole research can be summarized that the experiences, which can be understood as learning, school or not, create brain patterns that allow long-term, create new brain connections, which can help others coming and consolidate (Lois y Álvarez Buylla, 1992; Álvarez Buylla and Garcia, 2002; Bredy, Lin, Wei, Baker-Andersen, Mattick, 2011). 

References: 

 Aguilar, F. (2003 b) Plasticidad cerebral: parte 1. Rev Med IMSS. 41(1) 55-64.

Aguilar, F. (2005) Razones biológicas de la plasticidad cerebral y la restauración neurológica. Revista Plasticidad y Restauración Neurológica. Vol. 4 Num.1. 5-6.

Álvarez Buylla, A. & García Verdugo, J.M. (2002) Neurogenesis in adult subventricular zone. Journal of neuroscience. 22 (3) 629 - 634.

Bredy, TW., Lin, Q., Wei, W., Baker-Andersen, D., & Mattick, JS. (2011) MicroRNA regulation of neural plasticity and memory. Neurobiology of Learning and Memory. 96 (1) 89-94.

Díaz-Arribas, M., Pardo-Hervás, P., Tabares-Lavado, M., Ríos-Lago, M. y Maestú, F. (2006) Plasticidad del sistema nervioso central y estrategias de tratamiento para la reprogramación sensoriomotora: comparación de dos casos de accidente cerebrovascular isquémico en el territorio de la arteria cerebral media. Rev Neurol. 42 (3): 153-158.

Flores, J. (2005) Atención temprana en el síndrome de Down: Bases neurobiológicas  Rev Síndrome de Down 20: 132-142.

Lois, C. and Álvarez Buylla, A. (1992) Proliferating subvetricular zone cells in the adult mammalian forebrain can differentiate into neurons and glia. Proceedings of the National Academy of Science of the United States of America .90; 2074-2077.

Patchev, AV., Rodrigues, AJ., Sousa, N., Spengler, D., and Almeida, OFX. (2014) The future is now: early life events preset adult behavior. Acta Physiologica. 210 (1) 46-57.

Why is brain plasticity necessary ?

Brain development is based on genetic information and from a mechanism of adaptation to the environment. However, during the gestation period, since the uterine environment is very similar in the majority of individuals, the brain seems to grow based on genetic information, so it will be developing bases of the mechanisms that will be run later, that allow interaction with the external world. The genes that determine this polarity, are called organizers genes and they are not only expressed in the nervous system, but in other tissues and organs. While the genes that direct the differentiation-specific structures known as regulatory genes because they govern not only the anatomical structure but the function of the cells (Poch, 2001).

The reasons why the distribution of structures and the development agenda are preset are not very clear, but one theory is that the nature or complexity of the functions and the genetic programming can perhaps obey physical laws that govern other natural processes. In this sense Walsh and Diller (1981) explain that the brain maturity is a progression of neural development, which is determined by two types of neurons that built the kind of connections that are established between structures. On the one hand, pyramidal neurons (called macro neurons) differ from the neurons of local type, by which the first develop much earlier, establishing early connections then it will be difficult to restore after a brain injury, apparently these neurons are genetically clip-art and are running during birth, and they are responsible for establishing the functions of lower order, for example in the case of language, sound analysis and its phonological representation; while local neurons, will enjoy a longer liberty or plasticity and will be responsible to establish new connections in more advanced developmental periods. This type of neurons will be involved in the processes of higher order, is consolidating in a more progressive way and involved in functions such as semantic processing (Tubino, 2004).

In this way, brain plasticity mechanisms may include neurochemical changes, on cortex, receivers or structures, so it’s possible to say that functional plasticity is accompanied by structural plasticity, most important among the mechanisms of functional reorganization are the unmasking, the synaptic bud, the dendritic arborization, inhibition and facilitation and modification of neurotransmitters, among others, so it admits the possibility that there are several types of neuronal plasticity, which are considered to a) the developing brain plasticity; b) plasticity of the brain in learning period and c) plasticity in the adult brain (Aguilar, 2003).

Plasticity of the brain in development

Deacon (2002) explains about the plasticity of the brain in development, that during the period of embryogenesis genes are those who will determine the distribution of the different brain tissues and will also be responsible for the coordination of the processes that later will take place in the formation of the embryo, including the basic structures of the brain; but after the birth the genetic will run other mechanisms of brain structure that will largely depend on the environment both internal and external.

 

So at the beginning of the development of the nervous system, there is an excess of neural fibers, and an important part of the development process includes the neuronal trimming of excessive connections that are not necessary and may in fact be can be harmful to normal operation. 

In fact, thought this explosion of connections as early is part of the process of plasticity during development, and this has advantages of adaptation. However if any damage occurs during the period in which there are excessive and available connections, there are more possibilities of the system to survive despite the damage that you can design a route of alternate connections that may be suitable for the repair of the damage (Avaria, 2005).

It is so accepted that there are moments or critical periods in which each of the different areas of the central nervous system has special sensitivity and responsiveness to the changes induced by the different influences, and there is enough evidence about the influence of the experience affects most the final organization of the local circuits which to the main roads, because time has already completed the topographic organization of large circuits. 

But even if there is a period of particular sensitivity to receive sensory information that ultimately is going to influence and direct the learning, so although there is a certain structural predisposition that is set from the beginning and favors a previously established connection ans its maintain, this connection depends on the strength of the neuronal signals, as no matter where come from those signals but are retained and are finally established. However, is known that the age in which the injury occurred is one of the crucial factors to take into account to predict the course of brain injuries, as it has been found in research that focal lesions before one year of age will have a worse prognosis of intellectual function that injuries of the same type after that age (Riva & Cazzaniga 1986; Woods, 1980;  Tubino, 2004).

In this sense, since plasticity is greater in the first years of life, for most of the lesions and gradually decreases with age, the learning and the recovery will be enhanced if experiences are provided or stimuli early to the individual, especially in children, since the structures nerve in the first years of life are a maturation process that continuously new synaptic connections are established and growing myelination occurs their structures, so that in response to the stimuli coming from the experience, and by means of internal biochemical processes, the infant brain is forming. 

During this critical period, the circuits of the cerebral cortex have, as already mentioned, large capacity of plasticity, for which the absence of an adequate intake of stimuli, experiences or nutrients has important future functional consequences (Wash and Diller, 1981; Deacon, 2000; Hernandez-Muela, Mules, Mattos, 2004; Avaria, 2005).

 

Even when you know some of the factors that control the duration and the time that establishes these periods of special sensitivity, described that they relate to particular synaptogenesis, i.e., the phase in which there is hiperproducción of synapses in the cerebral cortex, but, as already explained, of these synapses will lose those neurons that do not establish any relevant connection finally will be eliminated by the system, giving rise to a phenomenon of remodeling of the brain network, so it is said that genetically predetermined development configures phases of production or synaptic outbreak (Wash and Diller, 1981).

However, there is evidence that not all the brain areas show periods of synaptogenesis and synaptic loss at the same time. In the primary visual cortex, for example there is an outbreak of synaptogenesis by 3-4 months of age with a maximum density at 4 months. But in the pre front cortex takes longer and reaches the synaptic density maximum to 3-5 years. The time course of the Elimination of synapses is also more prolonged in the frontal cortex (up to 20 years) than in the visual cortex (4 years); so, it is possible to affirm that maturation times for different brain structures are different, and the primary areas senso-motor cortical unfold before large areas of association. 

In this sense, el made that are necessary stages so that neural activity to complete development, involves the brain maturation is changed through his own stimulation and experience, providing the necessary adaptability to the brain. This scheme is probably cheaper from the biological point of view, since a model whereby the genetic control for the formation of all synapses is needed would require a incredible number of specific molecular markers and their respective genes, what a system rigid and dependent would do it. This is explained because of the extreme immaturity of the brain of the newborn, whose fragility justifies the total parental dependence of the newborn human. This emphasizes the total difference of man with respect to most of the animals, which even newborns, they are already capable of running many of its basic functions (Tubino, 2004).  

Also known that the ability to analyse and synthesize multiple sources of information, and generate different responses from the brain, which illustrates the centralized organization and brain function, there is a hierarchy in the organization in such a way that the lower segments carry out specific functions subject to the control and modulation of segments above, by which the complexity of the information processing increases progressively as the level becomes to up to the crust. But, from the periphery may cause, with certain stimuli, responses in higher levels that force the organization or the acquisition of certain functions. 

However, it has been particularly studied the early lesions that occur in the linguistic areas, which generally manage a good recovery function, but currently, there is extensive evidence that the process of recovery of functions is not able to completely eliminate the effects of the early focal lesions as in the case of the language, throughout the subsequent development of the infant, you can see difficulties in reading, writing, comprehension, articulation, fluency and/or syntax (Verger and Junque, 2000)

One possible explanation of this effect, is that all the sensory and motor regions primary brain are related from a functional point of view, by association fibers. Cortical association areas, for example, are directly connected among themselves, while the primary cortical areas are connected each other indirectly through the Association areas. Homologous areas in both hemispheres are connected through fiber inter hemispheric, mainly by the Corpus Callosum. This brain interconnectivity allows a constant interaction within each hemisphere and between both hemispheres, and in this way is intended to adapt responses globally and dynamics (Hernandez-Muela, Mules and Mattos 2004; Poch, 2001).

It is thus that the brain works in a coordinated manner and analyzes the world in a global way, for this reason, when you read something is to understand the letters that make up each word, understood the meaning of each of the words of a sentence, however, these processes are not synthesized independently, but that a general sense is given to each phrase. This is possible thanks to the coordination between each of the lobes of the brain, this is the engineering of the brain, which that allows you to interpret the world and the same design a spacecraft that learn the abc. East the working tool when it comes to learning, and modify their connections, is the final triumph of the teaching. 

It has be found at the same time, another important aspect that is modifiable during critical periods: cerebral laterality, this is expressed in three aspects: anatomical symmetry, unilateral functional differences (as the location of language, speech and analytical processing in the left hemisphere, and temporo-spatial skills, as those related to music and the emotional and humorous repertoire (right) and contralateral sensorimotor control, in this way, understand the functionality of the brain in these three aspects is essential to understand the processes that take place in the reorganization of the brain during the learning process because it is a very rich source of experiences that can benefit education (Maciques, 2004).

References:

 Aguilar, F. (2003) Plasticidad cerebral: parte 1. Rev Med IMSS. 41(1) 55-64.

Avaria, M. A. (2005)  Aspectos biológicos del desarrollo psicomotor.  Rev. Ped. Elec. [en línea] Vol 2, N° 1.

Deacon, T. (2000) Evolutionary perspectivas on language and brain plasticity. Cognitive science. 28 (1) 34- 39.

Hernández-Muela, S., Mulas, F. y  Mattos, L. (2004) Plasticidad neuronal funcional Rev Neurol. 38 (Supl 1): S58-S68.

Maciques (2004)  Plasticidad Neuronal. Revista de neurología. 2 (3) 13-17.

Poch, M.L. (2001) Neurobiología del desarrollo temprano. Contextos educativos. 4. 79-94.

Tubino, M. (2004) Plasticidad y evolución: papel de la interacción cerebro – entorno. Revista de estudios neurolingüsticos.Vol. 2, número 1. 21-39

Verquer, K. & Junqué, C. (2000) Recuperación de las lesiones cerebrales en la infancia: polémica en torno a la plasticidad cerebral. Rev Logop Fon Audiol. XX(3):151-157.

Walsh, T. M. & Diller, K. C. (1981) Neurolinguistic considerations on the optimum age of second language learning. En. K.C. Diller (Ed) Universal in language learning aptitude USA. Rowley: Newbury House Publishers.

Woods, B. (1980) The restricted effects of right hemisphere lesions after age one: Wechsler test data. Neuropsychology. 18: 65-70.

Brain plasticity: history of the concept

The term plasticity was introduced in 1890 by the American psychologist William James, in which described the natural modificability of human behavior. Although in the last years of the 19th century, Santiago Ramón y Cajal proposed that these behavioral modifications would surely have a anatomical substrate, attributable to the brain, and those changes of variable duration in synaptic function which arise with origin in external stimuli affecting learning, are modificable by this plasticity. Thus Lugaro and Ramón y Cajal deduced it almost at the same, with different variations of ideas, both explained that learning involves functional plastic changes in the properties of the neurons or their interconnections.

From this perspective, learning may be the result of a morphological change among the interconnections of nerve cells, similar to the phenomena that occur during the formation of synapses in the embryonic life, however, after Cajal’s death, it was adopted a rigid way of looking at the adult central nervous system and it was accepted the idea that once finished its development, anatomy of the brain remained unchanged, except for the degenerative processes (cited in Nieto, 2003). 

Since then, the concept of synaptic plasticity has come developed mainly in studies related to memory and learning.  

However, even after years evidence about the capacity of our brain to change its functions and to compensate some damage, the importance of this role has come to be appreciated only recently, since studies brain in late 19th century and early 20th focused on the identification of areas of specific performance which gave the idea of a brain that governs its functions in specific areas and thus the widespread idea in the psychology of learning must be obtained in specific periods of time. 

Some persons believe, this was thanks to Paul Broca, who in the mid-19th century, identified a certain area in the left frontal lobe-related to language, which was the starting point for the neurosciences focused strictly on localizations of processes. Since then, many others continued describing specific brain areas with specialized functions, such as Broadmann; who described them but with more and more improved of morphological techniques, architectural and neurochemical studies, researchers discovered more details of the brain structure and functional connections.

The enormous complexity of the brain may have contributed to the conceptual rigidity that  was developed in those years, since its organization was known within a whole, the anatomists had to sectorize such knowledge. This motivated to Broadmann to divide the cortex into 52 regions, and descriptions made by constituents showed them separate, and this gave another reason to believe in concept of a rigid, strictly divided brain. This, coupled with studies of connectivity and the absence of concrete evidence of regeneration in the brain (in contrast to organs like the liver which has the capability of mitotic cell duplication), led to believe that it was a body divided in compartments, not malleable (not plastic) and with little ability to recovery after injury, so few Anatomists, physiologists or clinical projected a concept of dynamic adaptability of the brain (Aguilar, 2003b; Poch, 2001, Aguilar, 2005).

Currently is kind of a simple accept that an adult 30 years old knows much more than a child of 10 years old, and at 70 years old someone knows more than during 20’s, because the cognitive development process goes hand in hand with developing brain in particular the development of adapted neural networks that allow respond to the environment, and all this depends on the genetic information which is endowed to each individual as well as from the mechanisms of adaptation of the environment, so these days, such assertions become searchable thanks to the study of the process called neuroplasticity or brain plasticity (Tubino, 2004 and Ginarte, 2007).

However, it was not until some years later that this concept of neuroplasticity was defined by Gollini (1981) and Kaplan (1983) as a potential of nervous system to change (although it has observed this same capacity in other systems such as the endocrine, respiratory and skeletal muscle). This capacity can modify behavior and allow the adaptation to the environment patterns of conduct, so this ability of central nervous system allows it to never be finished and always change and adjusting as result of the interaction of factors genetic and cultural, but also it’s know that this ability decreases as neurons specialize (Bergado cited in Ginarte, 2007; Poch, 2001).

 

Defined more broadly, plasticity is the functional adaptation of the central nervous system to minimize the effects of the structural or physiological alterations, regardless of the original cause. This is possible thanks to the faculty of the nervous system to experience structural-functional changes detonated by influences endogenous (internal) or exogenous (external), which can occur at any time of life. Some researchers explain that this includes learning in its entirety; more specifically, there is evidence of morphological changes such as neuronal branching after learn a new skill. 

 While another group of experts, with a more intermediate position, considered it as adaptive capacity of the central nervous system to modify its own structural and functional organization, since plasticity mechanisms may include neurochemical changes,  at the parenquima, receivers or structures. Likewise, functional plasticity is accompanied by a structural plasticity, since there is also evidence of cooperation between brain areas (Aguilar, 2003b).

In the same way, it has been observed that there is also a great ability to communicate between neuron-glia, which collaborates on brain plasticity (either by creating new connections or removal and cleaning of the existing) (Aguilar, 2003a, b).

 

In response, it should be recalled that major cellular kinds of nervous tissue are the neurons and glial cells. Neurons, cells that are highly specialized in quick, message reception and transmission have a small body and multiple branches that cover an extensive area, allowing you to optimize your intercom, making them malleable to the needs of the cerebral environment (Nieto, 2003).

It is thus that the synaptic strength can be altered in the different periods of development and range from milliseconds to months. 

The cellular mechanisms of these changes are transitional modifications of neurotransmission and in longer alterations, changes in gene expression, so it can be said that there is a continuous renovation of the organization and neuronal maturation (Aguilar, 2003a; Aguilar, 2003b; Castroviejo, 1996; Poch, 2001).

References: 

Aguilar, F. (2003 a) Plasticidad cerebral: parte 2. Rev Med IMSS. 41 (2) 133-142.

Aguilar, F. (2003 b) Plasticidad cerebral: parte 1. Rev Med IMSS. 41(1) 55-64.

Aguilar, F. (2005) Razones biológicas de la plasticidad cerebral y la restauración neurológica. Revista Plasticidad y Restauración Neurológica. Vol. 4 Num.1. 5-6.

Castroviejo, P. (1996) Plasticidad cerebral. Revista de Neurología 24 (135) 1361-1366.

Ginarte, Y. (2007) La neuroplasticidad como base biológica de la rehabilitación cognitiva. Geroinfo. Vol. 2. No. 1. 31-38

Gollin. E. S. (1981) Developmental and plasticity: behavioral and biological aspects of variation in developmental. New York. Academic Press.

Kaplan, B. A. (1983) Developmental psychology: historical and philosophical learning. New Jersey. Elrbaum Hillsdale.

Nieto, M. (2003) Plasticidad neural. Mente y cerebro. O3. 72-80.

Poch, M.L. (2001) Neurobiología del desarrollo temprano. Contextos educativos. 4. 79-94.

Tubino, M. (2004) Plasticidad y evolución: papel de la interacción cerebro – entorno. Revista de estudios neurolingüsticos. Vol. 2, número 1. 21-39