Friday, June 15, 2007
Neuroplasticity
Neuroplasticity (variously referred to as brain plasticity or cortical plasticity) refers to the changes that occur in the organization of the brain, and in particular changes that occur to the location of specific information processing functions, as a result of the effect of experience during development and as mature animals. A common and surprising consequence of brain plasticity is that the location of a given function can "move" from one location to another in the brain due to repeated learning or brain trauma.
The concept of plasticity can be applied to molecular as well as to environmental events. The phenomenon itself is complex and can involve many levels of organization. To some extent the term itself has lost its explanatory value because almost any changes in brain activity can be attributed to some sort of "plasticity". For example, the term is used prevalently in studies of axon guidance during development, short-term visual adaptation to motion or contours, maturation of cortical maps, recovery after amputation or stroke, and changes that occur in normal learning in the adult. Some authors separate forms into adaptations that have positive or negative consequences for the animal.
For example, if an organism, after a stroke, can recover to normal levels of performance, that adaptiveness could be considered an example of "positive plasticity". An excessive level of neuronal growth leading to spasticity or tonic paralysis, or an excessive release of neurotransmitters in response to injury which could kill nerve cells, would have to be considered perhaps as a "negative or maladaptive" plasticity.
The main thing to know is that even the adult brain is not "hard-wired" with fixed and immutable neuronal circuits. Many people have been taught to believe that once a brain injury occurs, there is little to do to repair the damage. This is simply not the case and there is no fixed period of time after which "plasticity" is blocked or lost. We simply do not know all of the conditions that can enhance neuronal plasticity in the intact and damaged brain, but new discoveries are being made all of the time. There are many instances of cortical and subcortical (thalamic!) rewiring of neuronal circuits in response to training as well as in response to injury.
There is solid evidence that neurogenesis, the formation of new nerve cells, occurs in the adult, mammalian brain--and such changes can persist well into old age. The evidence for neurogenesis is restricted to the hippocampus and olfactory bulb. In the rest of the brain, neurons can die, but they cannot be created.
To review, plasticity is the selective elimination of axons, dendrites, axon and dendrite branches, and synapses, without loss of the parent neurons, which occurs during normal development of the nervous system, as well as in response to injury or disease. The widespread developmental phenomena of exuberant axonal projections and synaptic connections require both small-scale and large-scale axon pruning to generate precise efficient connectivity. This pruning provides a mechanism for neural plasticity in the developing and adult nervous system, as well as a mechanism to evolve differences between species in a projection system.
Such pruning is also required to remove damaged axonal connections or those that are perceived by local mechanisms as not being efficient for the required circuit, to stabilize the affected neural circuits, and to initiate their maturation or repair. Pruning occurs through retraction, degeneration or functional degradation.
To maintain energy efficiency (whether the program is physiological or not), the CNS, through innate intelligence, will actually change the cells themselves!
