Neuroplasticity is the brain’s remarkable ability to reorganise itself by forming and eliminating neural connections throughout life. This adaptive capability is essential for learning, memory and recovery from brain injuries.
Neuroplasticity manifests in two ways: functional, and structural plasticity. Functional plasticity is the brain’s ability to move the capability of performing functions from damaged areas to undamaged ones. For example, after a stroke, other parts of the brain may take over the functions that were previously controlled by other areas. Meanwhile, structural plasticity involves the brain’s ability to physically change in structure, such as when learning, during experiences, or injury. It includes growth of new neurons (neurogenesis) and formation of new synaptic connections.
Mechanisms of neuroplasticity
1. Synaptic plasticity: changes in strength of the synapses (the connections between neurons) are crucial for learning and memory. Key processes involved are long-term potentiation (LTP) and long-term depression (LTD), strengthening or weakening synapses over time in response to increases or decreases in their activity.
Long-term potentiation (LTP) is a process that results in a lasting enhancement of signal transmission between two neurons when they are stimulated together and the strengthening of synaptic connections. This phenomenon is typically triggered by high-frequency stimulation of the synapse. The induction of LTP relies on the influx of calcium ions through NMDA receptors, which activates signalling pathways that boost synaptic strength. Both presynaptic and postsynaptic changes are involved in LTP, with increased neurotransmitter release from the presynaptic neuron and heightened receptor sensitivity or density on the postsynaptic neuron contributing to the overall enhancement of synaptic transmission.
Long-term depression (LTD) is a process that results in a sustained reduction in synaptic strength, usually induced by low-frequency stimulation of the synapse. This decrease in synaptic efficiency is characterized by the removal of neurotransmitter receptors, such as AMPA receptors, from the postsynaptic neuron. Unlike long-term potentiation, which involves an influx of calcium ions through NMDA receptors to strengthen synapses, LTD involves a lower influx of calcium, activating phosphatases that lead to receptor removal. Both presynaptic and postsynaptic changes contribute to LTD, including diminished neurotransmitter release from the presynaptic neuron and a decrease in receptor density or sensitivity on the postsynaptic neuron.
2. Neurogenesis: generation of new neurons, particularly in the hippocampus, which is vital for learning and memory.
3. Dendritic branching: the growth of dendrite branches at the end of axons enhances the formation of new connections.
Factors that influence neuroplasticity
1. Age: neuroplasticity is more pronounced in childhood; however, adults retain significant plasticity, especially in response to stimuli like learning new skills or rehabilitation after injury.
2. Environments with stimulating activities such as physical exercise, social interaction, cognitive challenges, and exposure to novel experiences enhance neuroplasticity. This is due to increased blood flow and providing complex varied stimuli.
3. Experience and learning leads to formation and strengthening of synaptic connections.
4. Physical activity promotes synaptic plasticity, benefiting cognitive functions.
5. Dietary nutrients, such as omega-3 fatty acids and antioxidants, support brain health and plasticity.
Neuroplasticity in health and disease
Memory consolidation techniques, such as spaced repetition, enhance long-term retention of information. Similarly, post-injury rehabilitation strategies aim to harness neuroplasticity to restore lost functions. These include physical therapy, cognitive rehabilitation, or constrain induced movement therapy, a rehabilitation technique that involves restricting the use of an unaffected limb to encourage the use and improve the function of a weaker limb, commonly used in stroke recovery. Neuroplasticity also plays a role in mental health conditions, e.g. CBT aims to rewire maladaptive circuits in depression and anxiety.
Outlook
In the future, there are multiple ways in which we can continue to harness neuroplasticity. Devices such as brain computer interfaces can directly influence neuroplasticity by providing real-time feedback and targeted stimulation, which helps the brain to reorganize and form new neural connections, thereby enhancing motor and cognitive functions. Pharmacological drugs, such as memantine (used for Alzheimer's disease), donepezil (an acetylcholinesterase inhibitor), and ketamine (an anaesthetic with rapid antidepressant effects) can promote neuroplasticity by modulating neurotransmitter systems, enhancing synaptic connections, and supporting cognitive and emotional function, and hence can be used to treat neurological disorders. Genes and their expression can also influence neuroplasticity.
In conclusion, neuroplasticity, the brain’s dynamic ability to adapt, learn, and heal, not only supports our cognitive and motor functions, but also gives us hope for recovery from injuries and treatment of neurological disorders. As research progresses, harnessing neuroplasticity enables us to unlock new discoveries, ultimately enhancing human health and wellbeing.
This article was written by Meghna Solanki and edited by Julia Dabrowska, with graphics produced by Lilly Green. If you enjoyed this article, be the first to be notified about new posts by signing up to become a WiNUK member (top right of this page)! Interested in writing for WiNUK yourself? Contact us through the blog page and the editors will be in touch.
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