Activity-dependent plasticity
Many scientists found it hard to receive funding because nearly everyone unanimously supported the fact that the brain was fully developed at adulthood and specific regions were unable to change functions after the critical period.
A similar experiment was reported again by Bach y Rita in 1986 where vibrotactile stimulation was delivered to the index fingertips of naive blindfolded subjects.
[7] He found that five sighted adult subjects recognized shapes across all sizes 79.8% of the time, a remarkable finding that has led to the incorporation of the tongue electrotactile stimulus into cosmetically acceptable and practical designs for blind people.
Another pioneer within the field of activity-dependent plasticity is Michael Merzenich, currently a professor in neuroscience at the University of California, San Francisco.
[9] While assessing the recorded changes in the primary somatosensory cortex of adult monkeys, he looked at several features of the data including how altered schedules of activity from the skin remap to cortical modeling and other factors that affect the representational remodeling of the brain.
Through many studies involving adaptive training exercises on computer, he has successfully designed methods to improve their temporal processing skills.
These adaptive measures include word-processing games and comprehension tests that involve multiple regions of the brain in order to answer.
[11] Alongside a team of scientists, Merzenich helped to provide evidence that autism probes monochannel perception where a stronger stimulus-driven representation dominates behavior and weaker stimuli are practically ignored in comparison.
These receptors exist at postsynaptic sites and along with the regulation of local inhibitory synapses have been found to be very sensitive to critical period alterations.
More specifically, integrins, which are receptors for extracellular matrix proteins and involved with CAMs, are explicitly incorporated in synapse maturation and memory formation.
In essence, it is the brain's ability to retain and develop memories based on activity-driven changes of synaptic strength that allow stronger learning of information.
It is thought to be the growing and adapting quality of dendritic spines that provide the basis for synaptic plasticity connected to learning and memory.
The Arc gene is activity-regulated[21] and the transcribed mRNA is localized to activated synaptic sites[22][23] where the translated protein plays a role in AMPA receptor trafficking.
[3] The mechanisms of activity-dependent plasticity result in membrane depolarization and calcium influx, which in turn trigger cellular changes that affect synaptic connections and gene transcription.
Each of the studies' findings aims to help proper development of the brain while improving a wide variety of tasks such as speech, movement, comprehension, and memory.
The changes in synaptic connections and strength are results from LTP and LTD and are strongly regulated by the release of brain-derived neurotrophic factor (BDNF), an activity-dependent synapse-development protein.
Another research model of activity-dependent plasticity includes the excitatory corticostriatal pathway that is involved in information processing related to adaptive motor behaviors and displays long-lasting synaptic changes.
The change in synaptic strength is responsible for motor learning and is dependent on the simultaneous activation of glutamatergic corticostriatal and dopaminergic nigrostriatal pathways.
[30] The two types of intellectual disability[clarification needed] related to plasticity depend on dysfunctional neuronal development or alterations in molecular mechanisms involved in synaptic organization.
After one year of crawling and unusual therapy tactics including playing basic children's games and washing pots, his father's rehabilitation was nearly complete and he went back to his role as a professor at City College in New York.
[31] This remarkable recovery from a stroke proves that even someone with abnormal behavior and severe medical complications can recover nearly all of the normal functions by much practice and perseverance.
Dr. Li and several others have actually identified the TRPV1 channel as a target to facilitate LTP and suppress LTD, therefore helping to protect the feature of synaptic plasticity and retention of memory from the effects of stress.
In addition to a better understanding of the various disorders, neurologists should and will look at the plasticity incurred by the immune system, as it will provide great insight into diseases and also give the basis of new immune-centered therapeutics.
[34] A better perspective of the cellular mechanisms that regulate neuronal morphology is the next step to discovering new treatments for learning and memory pathological conditions.
