Neuroplasticity is the ability of the brain to respond to stimulus through structural and functional changes. This trait has enabled humans to survive and evolve for thousands of years and is present across many instances of everyday life, from repetitive learning and practice to recovery from brain injury, the topic of this article.
The Neuron
Neuroplasticity is only possible through the neuron, cells that form connections across the brain and transmit signals to one another which govern your thoughts, behavior, and emotions. To break down this signaling process, let’s split it into two stages: electrical signaling and chemical signaling. During the electrical signaling stage, an impulse, or jolt of electricity will travel through the neruons, making its way through the cell body and down the axon until it reaches the axon terminal (See Neuron Diagram). Then, upon arriving to the axon terminal, the jolt of electricity will trigger the release of neurotransmitters, chemical messengers that float between neuron to neuron. Once the neurotransmitters leave the axon terminal, they will travel through the synapse (See Synaptic Transmission Diagram), an open space between neurons, and eventually be received by another neuron via the dendrites. Upon receiving the chemical signal, dendrites will trigger an electrical signal to pass through the second neuron, and the electrical to chemical signaling process will repeat again.
A Diagram of a Neuron
A Diagram of a Synapse
The presynaptic neuron passes the signal to the postsynaptic neuron.
Now that we’ve established the structure and function of the neuron, we can look into how neurons and neuroplasticity aid the brain in the healing process following injury.
How does neuroplasticity work to repair the brain after injury?
Brain injury, in addition to external damages (scrapes, cuts, broken bones), can also cause internal neuron death. Since neurons form the underlying circuits of connection within the brain, losing a bunch of them can restrict the ability of the brain to relay information to certain regions. This can cause the onset of issues ranging from memory impairment to a complete loss of motor skills depending on the severity of the injury.
There are multiple phases of neural activity that characterize the healing process of neuroplasticity.
1) Following the injury, cell death occurs and the activity within cortical inhibitory pathways decreases. The role of cortical inhibitory pathways is to regulate neuron activity in the cortex, playing an important role in continual learning and memory preservation. However, the key point is that this decrease in inhibition means that neural activity will increase, ultimately revealing new networks of neurons.
2) After 1-2 days, the activity of cortical inhibitory pathways will increase back to its standard level, as inhibition is necessary for the brain to function appropriately. New neurons and synapses will begin to form and restorative cells will be recruited to nurse the damaged region back to health.
3) In the weeks following the injury, axon sprouting is stimulated. With proper treatment, the brain can fully restore itself after a traumatic brain injury.
Diagram of the Process of Axon Sprouting
References
Barron, Helen C. “Neural inhibition for continual learning and memory.” Current opinion in neurobiology vol. 67 (2021): 85-94. doi:10.1016/j.conb.2020.09.007
Daskalakis, Zafiris J et al. “The role of cortical inhibition in the pathophysiology and treatment of schizophrenia.” Brain research reviews vol. 56,2 (2007): 427-42. doi:10.1016/j.brainresrev.2007.09.006
Evans, Olivia Guy. “Synapse: Definition, Parts, Types & Function.” Simply Psychology, 14 Feb. 2023, www.simplypsychology.org/synapse.html.
“Neuron Diagram & Types.” Arizona State University, askabiologist.asu.edu/neuron-anatomy. Accessed 31 May 2023.
Puderbaugh, Matt, and Prabhu Emmady. “Neuroplasticity.” National Library of Medicine, www.ncbi.nlm.nih.gov/books/NBK557811/.
Su, YouRong Sophie, et al. “Neuroplasticity after Traumatic Brain Injury.” National Center for Biotechnology Information, www.ncbi.nlm.nih.gov/books/NBK326735/.
Disclaimer: This information is intended for educational use only, and should not be construed as professional advice.