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Neuroplasticity

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Neuroplasticity reflects the brain's remarkable capacity to adapt and evolve, responding dynamically to learning, experiences, or injury by reorganizing its neural circuitry. This reorganization involves creating new neural connections and refining old ones through a series of biological processes that contribute to the brain's lifelong development and adaptability.

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Long-term Potentiation

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Long-term potentiation, or LTP, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTP is the process of synaptic strengthening that occurs over time between pre and postsynaptic neuronal connections. The synaptic strengthening of LTP works in opposition to the synaptic weakening of long-term depression (LTD) and together are the main mechanisms that underlie learning and memory.
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Plasticity during stroke recovery: from synapse to behaviour.

Timothy H Murphy¹, Dale Corbett

¹Kinsmen Laboratory, Department of Psychiatry, University of British Columbia, Vancouver, British Columbia, Canada. thmurphy@interchange.ubc.ca

Nature Reviews. Neuroscience

|November 6, 2009

Summary

Stroke damages brain networks, impairing function. Animal studies show a critical window for neuroplasticity after stroke offers the best chance for recovery by rewiring brain cells.

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Area of Science:

Neuroscience
Neurology
Regenerative Medicine

Background:

Stroke, caused by reduced brain blood flow, damages neuronal networks, leading to sensory, motor, or cognitive impairments.
Animal models indicate a transient period of enhanced neuroplasticity post-stroke, crucial for maximizing functional recovery.
Neuroplasticity involves activity-dependent neural rewiring and strengthening of synaptic connections.

Purpose of the Study:

To investigate optimal strategies for engaging and modifying surviving neuronal networks after stroke.
To identify methods for developing new response strategies to compensate for stroke-induced tissue loss.
To enhance functional recovery by leveraging the post-stroke neuroplastic window.

Main Methods:

Review of evidence from animal models of stroke.
Analysis of neuroplasticity mechanisms, including activity-dependent rewiring and synapse strengthening.
Exploration of therapeutic targets for modulating neuronal networks.

Main Results:

Confirmed the existence of a time-limited neuroplastic window post-stroke in animal models.
Highlighted activity-dependent rewiring and synapse strengthening as key plasticity mechanisms.
Identified the challenge in optimally engaging surviving neural networks for recovery.

Conclusions:

Optimally engaging and modifying surviving neuronal networks is critical for improving stroke recovery.
Developing targeted strategies to leverage the post-stroke neuroplastic window is essential.
Further research is needed to translate findings into effective human stroke rehabilitation therapies.