by Beatrice Awasthi
figures by Shreya Mantri

Loss of motor or cognitive skills can be a devastating after-effect of injury or illness. When things that used to feel easy suddenly feel impossible, a full recovery can appear completely out of reach. In many cases, persisting symptoms of pain, weakness, and fatigue can be due to dysfunction of the nervous system. Fortunately, the nervous system has an impressive ability to adapt and recover following traumatic events, a phenomenon known as neuroplasticity. Neuroplasticity allows people to regain abilities that were temporarily lost following a traumatic event. A better understanding of neuroplasticity and the mechanisms through which the nervous system rewires itself could pave the way for improved treatments that promote rehabilitation after trauma. This article will give an overview of some basic mechanisms underlying neuroplasticity and discuss how neuroplasticity can be integrated into rehabilitation protocols.

Introduction to the nervous system

The peripheral nervous system allows us to move and sense stimuli in the environment using specialized cells called neurons. These billions of neurons are organized into complex communication networks that connect the brain, spinal cord, and other areas of the body, and they are broadly categorized into three classes: sensory neurons, motor neurons, and interneurons. Sensory neurons collect information about the environment (such as temperature and texture), motor neurons coordinate movement, and interneurons connect sensory and motor neurons.

All neurons are composed of a cell body, dendrites, and axons. The cell body is the main part of the cell and contains the genetic material and most cellular machinery inside a structure called the nucleus. Dendrites are short, tree-like protrusions that extend from the cell body and receive stimulating signals from other neurons. Axons are single, long arms that carry nerve impulses to other neurons or body parts. Communication between two neurons typically occurs at the junction between the axon of one neuron and the dendrites of another, across a small gap called a synapse. The axon of the transmitting neuron releases a small signaling molecule called a neurotransmitter, which travels across the synapse and is bound by the dendrites of the receiving neuron. This binding can trigger changes within the receiving neuron, such as releasing its own neurotransmitters to stimulate another neuron. Contact of a dendrite with axons is mediated by tiny protrusions on dendrites called dendritic spines. (Figure 1)

Figure 1. This diagram shows two neurons within a neuronal network. Within a neuron, information is transmitted by electrical signals. Neurons communicate with each other using neurotransmitters, which are released from the tips of the axon of the transmitting neuron and bind to the dendrites of the receiving neuron.

Precise organization of neurons within networks is key to the effective coordination of bodily functions such as movement, thinking, and memory formation. For example, a very specific sequence of neuronal signals is required for a soccer player to pass the ball. Signals sent from sensory neurons in the eyes to the brain let the player notice that their teammate is open. Further signaling between neurons in the brain allows the player to decide to pass, and motor neurons in the brain send signals to the player’s muscles, allowing them to kick the ball. Injury or illness that damages any of the nerves involved in this movement may prevent the player from performing the action.

Mechanisms of synaptic plasticity

A variety of diseases and traumatic events can induce damage to neuronal networks and cause loss of physical or cognitive abilities, including neurological conditions like stroke and traumatic injuries to the brain or spinal cord. Fortunately, neuronal networks possess a remarkable capacity for rewiring, especially in the face of damage. (Figure 2)

Figure 2. Injury to a neuron can disrupt neuronal networks. In this example, a traumatic injury disabling neuron B prevents neuron D from receiving stimuli, potentially leading to loss of motor or cognitive abilities. However, damage can also cause the synaptic connections of non-injured neurons to be strengthened, such as the connection between A and D. These newly strengthened synaptic connections can help to compensate for lost connections, allowing for recovery of skills.

How can affected patients regain lost skills? Synaptic connections are extremely dynamic and largely operate within a “use-it-or-lose-it” framework. The more signaling that happens between two neurons, the more changes are induced within both neurons that stabilize a synapse and strengthen the synaptic connection between them. To visualize how this strengthening occurs, scientists at the University of California, Santa Cruz looked at the brains of mice under a microscope. The scientists found that when teaching mice a new skill, new clusters of dendritic spines formed within the first day. In most mice, new clusters continued to form while practicing the task over subsequent days. These clusters could respond in unison to incoming signals, enhancing the ability of the neuron to react to signals while performing the task. The scientists concluded that mastery of the new skill was primarily driven by new dendritic spines, while existing ones may have shaped the learning experience but were not as active during the learning process. Their findings suggest that repeated practice is essential to enhancing synaptic adaptation when learning a new skill and is therefore key to mastering it. (Figure 3)

Figure 3. Researchers showed that when teaching mice a new skill, new clusters of dendritic spines began to form and continued to form during repeated practice of that same skill.

Integrating neuroplasticity into rehabilitation

Understanding neuroplasticity and how repeated practice strengthens synaptic connections can make a major difference in the effectiveness of rehabilitation, as has been shown for strokes. Strokes are caused by blood clots or bleeding in the brain that can damage neuronal networks, leaving patients with physical and motor deficits. Numerous studies have shown that damage to the brain automatically induces neuronal network rewiring and formation of new synapses. Current stroke rehabilitation protocols aim to augment this rewiring by providing patients with structured exercises and drills to relearn lost skills. These protocols generally include intensive physical therapy to relearn motor skills and speech and language therapy to regain the ability to speak, as needed. These therapies may be supplemented with additional components in an effort to enhance neuroplasticity, such as mental practice with motor imagery. In this practice, the patient visualizes themselves successfully completing motor tasks. While scientists do not fully understand the biological mechanisms that make mental practice effective, one possible explanation is that visualization of a movement strengthens synaptic connections by repeatedly activating the motor circuitry necessary for that movement. Like with the mice, practice can rewire the brain – even if you’re only practicing in your head!

Aerobic exercise may also play a key role in stroke rehabilitation. In addition to helping individuals regain endurance and aerobic capacity, aerobic exercise – like brisk walking, running on a treadmill, or cycling – is thought to promote neuroplasticity. Specifically, aerobic exercise has been found to stimulate the release of special signals that facilitate synaptic strengthening; one group found that engaging in high-intensity cycling intervals immediately after learning a new skill enhanced long-term retention. While further research is needed to understand the mechanism by which aerobic exercise influences neuroplasticity and to determine the optimal type and amount of exercise for stroke patients, it holds promise as a tool to support brain rewiring.

While recovery from a traumatic event may feel impossible, neuroplasticity is a powerful ally. The brain is capable of incredible rewiring and there are many options for synaptic connections to regain what appear to be “lost” skills. For these skills, practice makes perfect – or, at least, enhances mastery – and leaves its mark within the networks of the brain.

Beatrice Awasthi is a PhD student in Biological and Biomedical Sciences at Harvard Medical School. Her research focuses on the effects of tissue context on growth factor signaling.

Shreya Mantri is a PhD student in Biological and Biomedical Sciences at Harvard Medical School.

Cover image by geralt from pixabay.

For more information:

  • Synaptogenesis, or the formation of new synapses, likely holds many clues to the mechanisms of synaptic strengthening. This review provides an overview of the process.
  • The principles of neuroplasticity are also central to mental health conditions, such as depression. You can learn more in this article.
  • Check out this article to read about how neuroplasticity links chronic pain and depression.

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