As in all developmental change, genetics and environment are in constant interaction coordinating “interplay of disintegration and renewal.”

Interesting example: Fish brains grow when they have to think more and shrink if they don’t 

Developmental Plasticity: Synaptic Pruning


“Over the first few years of life, the brain grows rapidly. As each neuron matures, it sends out multiple branches (axons, which send information out, and dendrites, which take in information), increasing the number of synaptic contacts and laying the specific connections from house to house, or in the case of the brain, from neuron to neuron. At birth, each neuron in the cerebral cortex has approximately 2,500 synapses. By the time an infant is two or three years old, the number of synapses is approximately 15,000 synapses per neuron (Gopnick, et al., 1999). This amount is about twice that of the average adult brain. As we age, old connections are deleted through a process called synaptic pruning.

Synaptic pruning eliminates weaker synaptic contacts while stronger connections are kept and strengthened. Experience determines which connections will be strengthened and which will be pruned; connections that have been activated most frequently are preserved. Neurons must have a purpose to survive. Without a purpose, neurons die through a process called apoptosis in which neurons that do not receive or transmit information become damaged and die. Ineffective or weak connections are “pruned” in much the same way a gardener would prune a tree or bush, giving the plant the desired shape. It is plasticity that enables the process of developing and pruning connections, allowing the brain to adapt itself to its environment.

Plasticity of Learning and Memory

It was once believed that as we aged, the brain?s networks became fixed. In the past two decades, however, an enormous amount of research has revealed that the brain never stops changing and adjusting. Learning, as defined by Tortora and Grabowski (1996), is ?the ability to acquire new knowledge or skills through instruction or experience. Memory is the process by which that knowledge is retained over time.? The capacity of the brain to change with learning is plasticity. So how does the brain change with learning? According to Durbach (2000), there appear to be at least two types of modifications that occur in the brain with learning:

  • A change in the internal structure of the neurons, the most notable being in the area of synapses.
  • An increase in the number of synapses between neurons.

Initially, newly learned data are “stored” in short-term memory, which is a temporary ability to recall a few pieces of information. Some evidence supports the concept that short-term memory depends upon electrical and chemical events in the brain as opposed to structural changes such as the formation of new synapses. One theory of short-term memory states that memories may be caused by ?reverberating? neuronal circuits — that is, an incoming nerve impulse stimulates the first neuron which stimulates the second, and so on, with branches from the second neuron synapsing with the first. After a period of time, information may be moved into a more permanent type of memory, long-term memory, which is the result of anatomical or biochemical changes that occur in the brain (Tortora and Grabowski, 1996).

Injury-induced Plasticity: Plasticity and Brain Repair


During brain repair following injury, plastic changes are geared towards maximizing function in spite of the damaged brain. In studies involving rats in which one area of the brain was damaged, brain cells surrounding the damaged area underwent changes in their function and shape that allowed them to take on the functions of the damaged cells. Although this phenomenon has not been widely studied in humans, data indicate that similar (though less effective) changes occur in human brains following injury.”



First three years:  “A baby’s brain in the first three months focuses on neural connections that enable seeing and hearing. After mastering that, the brain focuses more on language and speech production. Around the one year mark, the brain turns to higher cognitive functions. But higher-level brain function depends on the quality of lower-level circuits formed soon after birth. Babies need stimulating and responsive interactions to develop those lower-level circuits.”  Read: https://science.unctv.org/content/reportersblog/babies-neural-connections then Harvard’s site on BRAIN ARCHITECTURE

Teenage: Between ages 11 and 17, children’s brain waves reduce significantly while they sleep, a new study found. Scientists think this change reflects a trimming-down process going on inside teenagers’ brains during these years, where extraneous mental connections made during childhood are lost.” …  “The fact that there are more connections [in a child’s brain] allows things to be moved around,” Campbell told LiveScience. “After adolescence, that alternate route is no longer available. You lose the ability to recover from a brain injury, or the ability to learn a language without an accent. But you gain adult cognitive powers.”  (Read Clara Moskowitz’s report for Live Science,  March 23, 2009. “Teen Brains Clear Out Childhood Thoughts.” on line at: https://www.livescience.com/3435-teen-brains-clear-childhood-thoughts.html)

Life-Long Development of the Nervous System:  from Harvard’s site on Brain Architecture   

plasticity & effort of brain changes
plasticity & effort of brain changes over time 



NEUROPLASTICITY manifest in kindling and Learning.

“It may sound odd to suggest that epileptic seizure activity [associated with kindling] could relate to learning [associated with long-term potentiation, LTP], but its possible that the separate cascade of mechanisms constituting kindling and learning intersect and share a number of common mechanisms. For this reason both kindling and learning are viewed as phenomena of neuroplasticity.  Kindling was also the first neuroplasticity phenomenon suggested to be useful for studying memory processes (Goddard and Douglas, 1975).

In the end, kindling was surpassed by LTP as the neuroplasticity phenomena of choice for modelling memory processes, largely because LTP more closely approximated normal neural activity. However, although closer to normal firing patterns then kindling, LTP is still far from normal neural activity. …  This succession of neuroplasticity phenomena has made it important to understand how the various forms of plasticity like LTP and kindling are related (Reviews: Baudry, 1986Cain, 1989). …

In a odd way, kindling research has come full circle, re-connecting with Graham Goddard’s original discovery of the phenomenon while studying learning. Kindling’s return to its point of origin is not without differences however, and much of the understanding provided by kindling has led to direct advancements in the development of effective treatments for the neurological disease of epilepsy. As such, the study of kindling continues to play one of the more important roles in neuroplasticty research.” (http://hargreaves.swong.webfactional.com/kindle.htm )





The almost 100 billion neurons of the human brain exist in a vast ecosystem in which individual neurons in groups of varying sizes are in continual competition for the critical resources needed for their healthy metabolism. The pervasive phenomenon of neuroplasticity specifically enables competitively successful neurons or nuclei to control functions.   Pulling these ideas together, David Eagleman and Don Vaughn proposed the theory that we dream in order to sustain activity in visual areas that might otherwise have faded in influence in the dark–the “defensive activation theory” –they “…suggest that the brain preserves the territory of the visual cortex by keeping it active at night. … dream sleep exists to keep neurons in the visual cortex active, thereby combating a takeover by the neighboring senses. (of course dreams also involve engagement of other senses as well as vision) (see their reporting in  TIME  Feb 5, 2021:26-27 https://time.com/5925206/why-do-we-dream/       (Eagleman is a neuroscientist at Stanford University; Vaughn PhD is a neuroscientist at UCLA. – a collaborative report is available)