Neuronal Plasticity and Learning: Development, Process and Application

CIA-1

MPS 235: BIO CIA-I

Topic- Neuronal Plasticity and Learning.

Submitted by

Akhilesh Parab

Department of Psychology,

CHRIST (Deemed to be University),

Bengaluru

Academic Year

2019-20

1
Neuronal Plasticity and Learning: Development, Process and Application

Neuronal Plasticity and Learning: Development, Process and Application.

Abstract

The current research review explores on the concept of neuronal plasticity discussing its

historical roots along with the changes and development of the concept. The paper also mentions

about the structural and functional mechanisms involved in the neural changes. A link between

neuronal plasticity and learning is formed by glancing through some of the approaches and

studies that explored these concepts. Finally, the concepts were also applied to the field of

clinical psychology by exploring the learning of addictive behaviour as a product of neuronal

plasticity. Potential implications in the field of clinical psychology are mentioned in the end of

the paper along with recommendations for future research in the field.

Key Words: Neuronal Plasticity, Learning, Addictive Behaviour.

Introduction

The ability of the brain to change its structure or function in response to the internal and external

goals or constraints is termed as neuronal plasticity. (Pascual-Leone, Amedi, Fregni, & Merabet,

2005). William James is credited for being the first person to adopt this term for the changes in

the neural path for development of habits. The term plasticity has been flashing in the field of

brain science for over a century which refers to the changes suspected in the neural networks

which results in modification of behaviour which maybe short-term or long-term, maturation,

adjustments in response to a loss like brain damage.

Historical Roots of the meaning of Neuronal Plasticity.

2
Neuronal Plasticity and Learning: Development, Process and Application

Cajal speculated that the formation of new connections in neurons is a pre-requisite for learning.

(Cowan & Kandel, 2001) Later, Kornorski (1948) and Hebb (1949) proposed strengthening of

specific synapses fluctuate as a consequence of the activities between neurons. Well, the usage of

the term plasticity dates back to Freud (Centonze et al. 2004) where he used it with reference to

nervous system and learning followed by William James who addressed the issue of brain

plasticity from a modern perspective linking property of plasticity with behavioral habits along

with the repeated usage of the specific brain pathways. According to William James (1890),

plasticity in general is the phenomena seen in forming of habits in living beings in relation to the

organic materials of which their bodies are composed. He also developed this concept in which

he suggested that the simultaneously activated brain components could drain in to each other

resulting in the formation of the new association pathway. James missed the concept of synapse

in his theoretical assumptions, but they still have a modern touch as he speculates the

possibilities that; neuronal paths are constructed through use, simultaneous activity of the brain

components is responsible for the promotion of functional association, the concept of drainage

was because of the lowered resistance to conduction during functional activity.

The term synapse was given and indentified by Sherrington. He referred to it as the

device which is responsible for unidirectionality of the nerve signals in the neuronal pathways

(Sherrington, 1897, 1900, 1906). Sherrington missed on the aspect of elaboration of the possible

relations between learning and synaptic plasticity. The very first hypothesis about associative

memories and motor-dependent skills depending on the synaptic transmission of a localized area

of the brain was given by Tanzi in 1893 which was 4 years prior to the appearance of the term

synapse. Tanzi and Lugaro (her student) were convinced with Cajal’s view of the presence of

tiny gaps between two neurons. Lugaro (1898a, 1905, 1909) extended on Tanzi’s hypothesis

3
Neuronal Plasticity and Learning: Development, Process and Application

using the term plasticity to practice related changes in the synapse. Cajal was among the arly

pioneers in laying the concept of neural plasticity and the term plasticity who proposed cortical

changes to be associated with learning back in 1982. Cajal also published a paper suggesting the

plasticity of cell processes is likely to change among various life periods; high in young children,

decreasing in adults to vanishing in the old age. Many names came in this field to be the

proponents in the evolution of the concept, but one person who took this concept of neural

plasticity to a long way after the publishing the organization of behaviour (Hebb, 1949).

Neuronal circuits are also called Hebbian in honor for the major theoretical contributions made

by him to the field. Hebb (1958) in his writings emphasized the need for psychologists to be

updated with the recent neurophysiological research and vice-versa. The synaptic plasticity

theory of learning was rehabilitated in the late 1940s when Konorski and particularly Hebb

argued successfully that there was no better alternative way to think about the modifiability of

the brain by experience and practice. Hebb’s 4euroimagin hypothesis about the mechanism of

adult learning contained elements strikingly similar to the early speculations of James, Tanzi and

Cajal.

Modern view of neuronal plasticity.

It is the ability of the neurons to change in its structure and function as a response to the changes

in their environment. Neurons are parts of the circuits in the brain and neurons have the ability to

change its roles by altering its responses to the input as well as by influencing other neurons.

Strengths of the connections in synapse are responsible for neural plasticity. It is important for

the normal development of the brain circuits. Synaptic plasticity is the reason that makes people

different from each other by the differences in the brain circuits. Neural plasticity is pretty much

associated with memory, skill, learning, recovery from a brain injury. (Kaas, 2001) Plasticity on

4
Neuronal Plasticity and Learning: Development, Process and Application

the other continuum is also responsible for certain maladaptive behaviour, psychological

disorders as a biological cause to it. A complete understanding of plasticity is useful as it will

give a clear picture of when to promote it when it is beneficial and control it when it might be

harmful. Zif268 is a transcription regulatory protein responsible for the expression and function

in a context of neuronal activity is considered to be tightly linked to neuronal plasticity. Basic

mechanisms that are involved in plasticity include neurogenesis, programmed cell death, and

activity‐dependent synaptic plasticity. Repetitive stimulation of synapses can cause long‐term

potentiation or long‐term depression of neurotransmission. Together, these changes are

associated with physical changes in dendritic spines and neuronal circuits that eventually

influence behavior. These same mechanisms stand out as important contributors to the

developing brain’s ability to acquire new information, adapt to the rapidly changing environment

and recover from injury (Johnston, 2009).

Structural and functional mechanisms of neural changes.

Increases in the cortical grey matter as a result of the complex array of morphological changes

including the synaptic events such as forming new connections and altering the strength of the

existing connections was seen in animal studies (Chklovskii et al., 2004; Dragnaski & May,

2008; Hirata et al., 2004). Increases in the size of the soma and nucleus of neurons, glia and

capillary dimensions influence the cortical morphology when animals were exposed to enriched

environment (Kozorovitskiy et al., 2005; Muotri & Gage, 2006). The morphological substrates of

long-term potentiation and long-term depression (Draganski & May, 2008), synaptic pruning

(Huttenlocher, 1979), changes in gene expression (Kleim et al., 1996), protein synthesis and

dendrite density (Comery et al.,1995) are all the changes in the synaptic contacts which are

included mechanisms linked with training and experience-related plasticity.

5
Neuronal Plasticity and Learning: Development, Process and Application

Hebb’s model of learning.

Hebb’s model works on the principle that “Neurons that fire together, wire together”. Hebb

postulates that when axon of cell one is in proximity to stimulate cell two and this stimulation

happens in a repetitive and a continuous fashion then it allows for some metabolic processes in

one or both the cells thereby forming a neural connection. Analogy of the grooves on a hill can

be taken that gets deep as more water flows down them, the grooves here are neural connections

and water is the electrical and chemical messages travelling through the neural network (Calbet,

2018).

Neuronal plasticity and learning.

The relation between neuroplasticity and learning is in such a way that when we learn, we form

new pathways in the brain. Every experience has the capacity to connect new neurons and

change our brain’s default way of operating. Of course, not all learning has the advantage of

neuroplasticity. For eg. Learning new facts, but learning a new language or a musical instrument

certainly does. It is through this sort of learning that we may be able to understand the process of

intentionally and purposefully rewiring the brain. Each neuron in an infant’s brain has about

7,500 connections with other neurons; By the age of 2, the brain’s neurons have more than

double the number of connections in an average adult brain (Mundkur, 2005). These connections

are slowly pruned away as the child grows up and starts forming their own unique patterns and

connections. The four main types of neuronal plasticity observed in children are; Adaptive in

which changes that occur when children practice a special skill and allow the brain to adapt to

functional or structural changes in the brain (like injuries); Impaired in which changes occur due

to genetic or acquired disorders; Excessive in which the reorganization of new, maladaptive

pathways that can cause disability or disorders; Plasticity that makes the brain vulnerable to

6
Neuronal Plasticity and Learning: Development, Process and Application

injury in which harmful neuronal pathways are formed that make injury more likely or more

impactful (Mundkur, 2005). These processes are stronger and more pronounced in young

children, allowing them to recover from injury far more effectively than most adults. In children,

profound cases of neuroplastic growth, recovery, and adaptation have been reported.

Various approaches and studies supporting neuronal plasticity and learning.

Cross‐sectional approach is most popularly used strategy to study neuroplasticity and learning in

which individuals with different levels of a given skill are compared and differences in neural

structure or function related to their skill level are identified. It is often used in developmental

and/or clinical developmental studies. For instance, in a study which measured structural change,

Elbert et al. (1995) found that musicians showed larger cortical representations and that the

extent of this representation was correlated with the age at which the person had begun to play in

contrast to non-musicians. Functional Imaging Literature also uses this approach, many studies

have showed distinct neural activation patterns across age that correspond to differences in

cognitive ability (Bunge et al. 2002; Casey et al., 1997; Durston et al., 2002; Luna et al., 2001;

van Leijenhorst et al., 2007). This approach has a limitation in terms of its statistical power but

the pros of savings in costs and time and being relative to longitudinal approach still makes it a

go to option (Kraemer et al., 2000). A major limitation to this approach is the vulnerability of the

confounding effects of the extraneous variables. (Kraemer et al., 2000). Also, there is a presence

of cohort effects in which individual variation in factors other than the factors of interest will

affect the results. (Poldrack, 2000).

7
Neuronal Plasticity and Learning: Development, Process and Application

Longitudinal approach is the second strategy in which participants are examined multiple

times over the course of learning. Training is an experience dependent process which uses

saturation to flood the organism with a particular experience. In one study using this approach

rats were trained on a changing series of patters in the Hebb‐Williams maze during a period of

25 days (Greenough et al., 1979) to examine the structural changes. Visual cortex of trained

animals was found to have two types of neurons had more dendrites in comparison with the non-

trained animals, while a third neuron type remained unchanged. Thus, these findings

demonstrated the specific and robust effects of learning through training on synaptic connectivity

While assessing the humans functional neurological activation cognitive tasks are used prior t,

later or during the training and this is then compared with a basel-line control task which is

performed without training. (Karni et al., 1995; Karni & Sagi, 1993). Determination of the

change in brain activity in association with the training is done. The main advantage to this

approach is that it provides optimal power to identify neural changes associated with the

experience of interest because it is within‐subject. However, a limitation logistically challenging

and expensive nature of longitudinal work, practice effects could potentially confound the

results.

Utility of Transcranial Magnetic Stimulation (TMS) in the field of neuroplasticity have

come in to the picture after the recent advances made in the tool. Since its introduction, it has

been known that repeated TMS (rTMS) of the motor cortex in healthy adult human participants

can lead to relatively lasting effects (usually of the order of 30–60 minutes) on the excitability of

the corticospinal output (Rothwell, 2007; Siebner and Rothwell, 2003). For instance, a recent

study showed that rTMS delivered to the superior temporal cortex causes macroscopic cortical

changes in gray matter in the auditory cortex as early as within 5 days of continuous intervention

8
Neuronal Plasticity and Learning: Development, Process and Application

(May et al., 2007) and work in patient populations has also uncovered the utility of this tool in

investigating plasticity in the diseased brain (Rothwell, 2007). Collectively, these approaches

highlight the utility of Neuroimaging tools in studying human neural plasticity.

Application: Neuronal plasticity and learning in the field of clinical psychology.

Neuronal plasticity and acquiring addictive behaviour. Neuroplasticity is the ability

of the brain to change, modify or inhibit certain neural connections in the brain. Addictive drugs

pharmacologically produce changes in the brain function which regulates how a person makes

sense and responds to the stimuli related to motivation. Thus, these make changes in the brain

circuits that allows us to learn and adapt to the important environmental stimuli like approaching

rewards (like food or sex) or to avoid dangerous situations (Kelley, 2004; Everitt & Robbins,

2005). The change in the motivational circuitry, the addictive substances impair the development

of behavioural strategies and progress towards behaviour of drug seeking and taking strategies

(Kalivas & Volkow, 2005). The release of dopamine makes the effect of drug salient, creating an

internal sense of importance of the behavioural response of taking the drug. The release of the

dopamine through addictive drugs is much greater in amplitude and duration. The article also

suggests that there is a relation between increased dopamine transmission and learning

behaviours to gain benefits or rewards which implies that release of dopamine is significant to

facilitate learning. Many studies also show that inhibiting the transmission of dopamine

decreases motivation and learning and stimulating it will lead to acquisition of learned

behaviours. Dopamine also functions as a signal or an indicator for the arrival of a reward by the

conditioned stimuli (Schultz, 1998). For example: In Pavlov’s example the ringing of the ringing

of the bell would sign the dogs to fire the dopamine cells, preparing the animal to start the

adaptive food-seeking response. Hence, continuous associations between the environment

9
Neuronal Plasticity and Learning: Development, Process and Application

stimuli and the dopamine release from the addictive drugs results in the environment stimuli

becoming the conditioned stimuli. This new form of learning is also attributed to neuroplasticity

as the brain is forming new connections on the basis of the proximity of firing. Also, now these

environmental stimuli cause in the release of dopamine to cue the person for drug-seeking

behaviour (i.e. relapse). There is a transition from prefrontal circuitry to habit motor circuitry

which signifies a loss of control leading to a compulsive relapse. Some 10euroimaging studies

indicate that reduced response to biological rewards in addicts is a reduction in dopamine

receptor activation in response to low doses of psychostimulants (Volkow et al. 2004, 2005).

Pharmacotherapies facilitate the capacity of addicts to include more declarative, decision-making

processes in relapse which is important to decrease compulsive relapse. Drugs that alter the

transmission of dopamine, glutamate or GABA are potential candidates for drug-seeking drives.

Mindfulness meditation and neuroplasticity. The findings from a research study on the

brain and meditation done on Dalai Lama recruited Tibetan Buddhist monks using brain-imaging

techniques suggest that long-term practitioners had actually altered the structure and function of

their brains (Davidson, 2010). Another study done on business people showed a shrinking size of

amygdala with a reduced activity in the brain as compared to the control group who didn’t

practice mindfulness (Wilson, 2013). Increased activity of the anterior cingulated cortex (closely

associated with the PF cortex) which results in greater emotional stability and less reactivity

(Wilson, 2013). Mindfulness meditation with the backing of the evidence of neuroplasticity can

be used to develop a treatment in clinical settings for psychological disorders.

10
Neuronal Plasticity and Learning: Development, Process and Application

Conclusion.

The research review gives a comprehensive understanding of neuronal plasticity and learning.

Using previous researches, it validates the link between the two concepts. The potential link

between the two concepts is supported through theoretical understanding and the development of

the concept. The potential applications of neuronal plasticity and learning to the field of clinical

psychology are discussed in the end of the paper. Previous researches are mainly focused on the

process of neuronal plasticity to acquire certain symptoms of psychopathology in developing a

disorder for eg. Addiction. Future research in the domain of neuronal plasticity can be focused

on the changes in the brain after certain treatment or interventions. This will in turn help us to

use neuronal plasticity as a tool of benefit in the field of clinical psychology.

11
Neuronal Plasticity and Learning: Development, Process and Application

References.

R, Brown., & P, Milner. (2003) The legacy of Donald O. Hebb: more than the Hebb Synapse.

Journal of Nature Reviews Neuroscience. 4:12. 1013-1019. doi: 10.1038/nrn1257

P, W. Kalivas., & C, O’Brien. (2008) Drug Addiction as a Pathology of Staged Neuroplasticity.

Journal of Neuropsychopharmacology, 33:1, 166-180. doi: 10.1038/sj.npp.1301564

T, Chen., M, Hauser., T, Simpatico., J, Femino., E, R. Braverman & D, Barh. (2012) The

Addictive Brain: All Roads Lead to Dopamine. Journal of Psychoactive Drugs, 44:2,

134-143. doi: 10.1080/02791072.2012.685407

M, B. Jensen. (2014, February 3) Neuroplasticity. Retrieved from:

https://www.youtube.com/watch?v=J8wW1t1JqUc&list=PLIVxyLLNA7G5Axx5aXZl5

QhW1ewtxt26H

M, Field., & W, Cox. (2008) Attentional bias in addictive behaviours: A review of its

development, causes, and consequences. Journal of Drug and Alcohol Dependence.

97(2), 1-20. doi: 10.1016/j.drugalcdep.2008.03.030

B, Everitt., & T, Robbins. (2005) Neural systems of reinforcement for drug addiction: From

actions to habits to compulsion. Journal of Nature Neuroscience. 8(11), 1-10. doi:

10.1038/nn1579

Berlucchi, G., & Buchtel, H. A. (2008). Neuronal plasticity: historical roots and evolution of

meaning. Experimental Brain Research, 192(3), 307–319. doi:10.1007/s0022100816116

12
Neuronal Plasticity and Learning: Development, Process and Application

Knapska, E., & Kaczmarek, L. (2004). A gene for neuronal plasticity in the mammalian brain:

Zif268/Egr-1/NGFI-A/Krox-24/TIS8/ZENK? Progress in Neurobiology, 74(4), 183–211.

doi:10.1016/j.pneurobio.2004.05.007

Wilson, A. (May 16, 2013). Mindfulness Meditation and the Brain. Huffington Post. Retrieved

from http://www.huffingtonpost.com/kripalu/mindfulnessmeditation_b_3238677.html

Davidson, R. J. & Lutz, A. (January, 2008). Buddha’s Brain: Neuroplasticity and Meditation. In

the Spotlight. Retrieved from

http://brainimaging.waisman.wisc.edu/publications/2008/DavidsonBuddha IEEE.pdf

Ackerman, E. A. (October, 2019). What is Neuroplasticity? A Psychologist Explains. Body and

brain. Retrieved from: https://positivepsychology.com/neuroplasticity/

Holzel, B. K., Camody, J., Evans, K. C., Hoge, E. A., Dusek, J. A., Morgan, L., Pitman, R. K., &

Lazar, S. W. (March, 2010). Stress Reduction Correlates with Structural Changes in the

Amygdala. US National Library of Medicine National Institutes of Health. Retrieved

from http://www.ncbi.nlm.nih.gov/pubmed/19776221

13