The brain's ability to reorganize itself by forming new neural connections throughout life. Neuroplasticity allows the neurons (nerve cells) in the brain to compensate for injury and disease and to adjust their activities in response to new situations or to changes in their environment. Brain reorganization takes place by mechanisms such as "axonal sprouting" in which undamaged axons grow new nerve endings to reconnect neurons whose links were injured or severed. Undamaged axons can also sprout nerve endings and connect with other undamaged nerve cells, forming new neural pathways to accomplish a needed function.

In 1793, Italian anatomist Michele Vicenzo Malacarne described experiments in which he paired animals, trained one of the pair extensively for years, and then dissected both. He discovered that the cerebellums of the trained animals were substantially larger. But these findings were eventually forgotten. The idea that the brain and its function are not fixed throughout adulthood was proposed in 1890 by William James in The Principles of Psychology, though the idea was largely neglected. Until around the 1970s, neuroscientists believed that the brain's structure and function was essentially fixed throughout adulthood.

While the brain was commonly understood as a nonrenewable organ in the early 1900s, Santiago Ramón y Cajal, father of neuroscience, used the term neuronal plasticity to describe nonpathological changes in the structure of adult brains. Based on his renowned Neuron doctrine, Cajal first described the neuron as the fundamental unit of the nervous system that later served as an essential foundation to develop the concept of neural plasticity. He used the term plasticity in reference to his work on findings of degeneration and regeneration in the central nervous system after a person had reached adulthood, specifically. Many neuroscientists used the term plasticity only to explain the regenerative capacity of the peripheral nervous system, which Cajal's conceptual transfer of the term gave rise to a controversial discussion.

While the fidelity of sensory inputs has long been known to affect perceptual development, the potential effects of weak, absent, or noisy sensory inputs on mature brain function are only beginning to be understood. Sensory information reaching the brain can be degraded due to exogenous or endogenous factors. Exogenous factors are environmental noise that reduces the discriminability of a stimulus, such as listening to a voice in a crowded room, whereas endogenous factors refer to limits of the peripheral sensory organs or central processing disorders that affect the perception of sensory inputs. In all cases, plastic processes determine how the brain responds and adapts to these challenging perceptual situations and a major goal of neuroscience research should be to understand and integrate our knowledge of these different contexts.

Regards
Meria Den
Managing Editor
Stroke Research & Therapy