Neuroplasticity improves Learning and Memory

Neuroplasticity improves Learning and Memory

Our brain’s ability to delete older neuronal synaptic networks while editing and generating newer networks improves learning and memory. The more neuronal synapses that are activated can increase our learning ability. These synaptic triggers can alter pre-existing networks for better efficiency or create new neuronal connections for overall density. 

Synaptic transmission occurs when something new is learned, and immediately ‘sent’ to short-term memory. Short term memory impulses then electrochemically transform into long-term memories through reverbration. The brain is a massive neuro-communication center. It is constantly learning and remembering, building new and negating old synaptic connections. Through learning to focus, to be totally aware of your mental, emotional and physical state of being, and knowing that you can achieve the desired brainwave state at will, is the basis of brainwave focus training.

Learning affects the brain in two different ways, neither of which would be possible without the unique plasticity of our brains. In response to a new experience or novel information, neuroplasticity allows either an alteration to the structure of already-existing connections between neurons, or forms brand-new connections between neurons. The latter leads to an increase in overall synaptic density, while the former merely makes existing pathways more efficient or suitable. In either way, the brain is remolded to take in this new data and, if useful, retain it. While the precise mechanism that allows this process to occur is still unclear, many researchers theorize that long-term memories are formed successfully when something called “reverbration” occurs. When we are first exposed to something new, that information enters our short-term memory, which depends mostly upon chemical and electrical processes known as synaptic transmission to retain information, rather than deeper and more lasting structural changes such as those mentioned above. The electrochemical impulses of short-term memory stimulate one neuron, which then stimulates another. The key to making information last occurs only when the second neuron repeats the impulse back again to the first. This is most likely to happen when we perceive the new information as especially important or when a certain experience is repeated fairly often. In these cases, the neural “echo” is sustained long enough to kick plasticity into high gear, leading to lasting structural changes that hard-wire the new information into the neural pathways of our brains. 

These changes result either in an alteration to an existing brain pathway, or in the formation of an all-new one. In this way, the new information or sensory experience is cemented into what seems, at its present moment, to be the most useful and efficient location within the massive neurocommunication network. Further repetition of the same information or experience may lead to more modifications in the connections that house it, or an increase in the number of connections that can access it as a result of the amazing plasticity of our brains.

Neuroplasticity is the saving grace of the damaged or disabled brain. Without it lost functions could never be regained nor could disabled processes ever hope to be improved. Plasticity allows the brain to rebuild the connections that, because of trauma, disease, or genetic misfortune, have resulted in decreased abilities. It also allows us to compensate for irreparably damaged or dysfunctional neural pathways by strengthening or rerouting our remaining ones. While these processes are likely to occur in any number of ways, scientists have identified four major patterns of plasticity that seem to work best in different situations. Take the case in which healthy cells surrounding an injured area of the brain change their function, even their shape, so as to perform the tasks and transfer the signals previously dealt with by the now-damaged neurons at the site of injury. This process, called “functional map expansion,” results in changes to the amount of brain surface area dedicated to sending and receiving signals from some specific part of the body. Brain cells can also reorganize existing synaptic pathways. This form of plasticity, known as a “compensatory masquerade,” allows already-constructed pathways that neighbor a damaged area to respond to changes in the body’s demands caused by lost function in some other area. Yet another neuroplastic process, “homologous region adoption,” allows one entire brain area to take over functions from another distant brain area (one not immediately neighboring the compensatory area, as in functional map expansion) that has been damaged. And, finally, neuroplasticity can occur in the form of “cross model reassignment,” which allows one type of sensory input to entirely replace another damaged one. Cross-model reassignment allows the brain of a blind individual, in learning to read Braille, to rewire the sense of touch so that it replaces the responsibilities of vision in the brain areas linked with reading. One or several of these neuroplastic responses enable us to recover, sometimes with astonishing completeness, from head injury, brain disease, or cognitive disability.