Brain plasticity refers to the observation that both the structure and function of the brain are molded by experience much in the way that plastic is shaped by a manufacturer to suit various demands. Brain plasticity occurs during development of the nervous system, when we learn, and in response to injury. This plasticity is manifested not only by neurons, the principle information-processing cells of the brain, but also by supportive elements including glial cells and the cells that comprise the vascular networks of the brain.
Developmental Versus Adulthood Plasticity
Greenough and his colleagues (1987) have proposed that plasticity in the developing and adult nervous system is similar in form but different in expression. During development, they note that there is a massive overproduction of neurons and synapses (connections between neurons) that are later pruned by experience. They propose that this type of plasticity may be characterized as “experience-expectant.” That is, the nervous system has been programmed by our genes to display an exuberant growth of connections at particular points in time (e.g., eye-opening) in anticipation of experiences that are common to the species. For example, all humans can expect to be born into a world that is visually rich. Our genes, therefore, direct visual centers of the brain to be created in which there are neurons capable of processing visual information (shape, color, movement). However, our genes do not know which type of visual information we will encounter, so the system is programmed to account for all possibilities. Once we open our eyes and start to examine our visual world, the brain prunes away those extra connections and neurons that are not necessary in our particular environment. If we were born into an environment that lacked horizontal lines, our nervous system would retain those neurons and synapses that process vertical lines, color, and movement but would remove those that are responsible for encoding horizontal lines. In contrast, “experience-dependent” plasticity occurs in adulthood in response to novel situations. Plasticity in this case is manifested by smaller bursts of new synaptic growth within localized regions of the brain that is then pruned by the continuing experience. For example, an adult that learns to play the piano would add new synapses in motor regions of the brain that control finger movement. As the adult becomes more practiced, some of these new synapses would be pruned away, leaving only those that provide for coordinated movement.
Experience-Induced Plasticity Of Neurons
Studies of brain plasticity indicate that characteristic changes include alterations of neuronal number, cell body (soma) size, dendritic extent and morphology, composition of the cellular membrane, and connectivity with other neurons (synapses). For example, several reports indicate that animals engaging in prolonged exercise exhibit increased neuronal proliferation (neurogenesis) and survival in the hippocampus. Other studies have consistently reported that the rearing of animals in an enriched environment produces substantial increases in brain volume (around 25%). This increase is distributed across areas of the brain (motor cortex, visual cortex, cerebellum) but is largest in visual cortex. Subsequent studies have indicated that this volume increase is accompanied by increases in the size of dendritic trees, increased numbers of synapses per neuron, and changes in the shape of presynaptic and postsynaptic elements.
A Model Of Brain Plasticity
Many neuroscientists have hypothesized how experience might promote brain plasticity and modify neuronal output. One of the most influential scientists was Donald O. Hebb, who proposed that the ability of two neurons to communicate with each other should be strengthened if those two neurons are repeatedly active at the same time. A physiological demonstration of this phenomenon was discovered in the early 1970s by Bliss and Lomo and was termed “long-term potentiation.”
Long-term potentiation (LTP) is a long-lasting increase in the excitability of a cell following a high frequency burst of stimulation. Many neuroscientists believe that LTP is a good model for the electrophysiological and structural changes that occur during development and in response to learning. It has most often been studied in the hippocampus, a brain structure strongly believed to play a role in learning and memory. In the hippocampus, LTP occurs when stimulation of afferent pathways causes release of the neurotransmitter glutamate. Glutamate binds to receptors (protein docking sites) on the postsynaptic neuron. Binding of the neurotransmitter opens ion channels that then permit sodium to enter the cell. Movement of the sodium ions into the cell induces a change in the membrane voltage of the neuron. This voltage change in the membrane, if sufficiently large, promotes the expulsion of an ionic blockade by magnesium of a second type of neurotransmitter receptor known as the NMDA receptor. Following the removal of the magnesium blockade, the neurotransmitter glutamate can freely bind to the NMDA receptor and open ion channels for calcium. Increased intracellular calcium triggers a cascade of events including the activation of enzymes that modify existing cellular proteins and that also trigger the synthesis of new proteins. Collectively, these events promote increases in neurotransmitter release from the presynaptic neuron as well as postsynaptic changes in the composition of the membrane and dendrites (e.g., exposure and/or creation of more glutamate receptors, the formation of more synapses, or larger synapses). The net effect of these events is a relatively permanent change in the excitability of the neuron. For example, hippocampal LTP induction is associated with a 100% to 200% increase in the size of extracellularly recorded field potentials in as little as 10 to 15 minutes after the application of the tetanus. This increase in field potential amplitude is long lasting.
Vascular Plasticity Of The Brain
The primary focus of morphological studies of brain plasticity has centered on changes in the quality or quantity of synaptic connections. Recent investigations, however, have observed that the growth of new blood vessels from existing capillaries, or angiogenesis, occurs in response to behavioral manipulations that involve extensive physical exercise. In these studies, rats were trained on a running wheel for 30 days and the cerebellar cortex and motor cortex were dissected and the density of capillaries was determined. These investigations found that capillary density increased approximately 25% in the exercised rats compared to inactive controls. This demonstration of angiogenesis in the adult mammalian brain is especially significant given that early reports suggested that cortical angiogenesis in the rat is complete by
21 days of age. More recent reports of cerebral cortical angiogenesis in adult rats placed in complex environments, undergoing exercise, or exposed to hypobaric hypoxia indicate that the capacity for cortical angiogenesis, while diminishing with age, continues at least into the second year of life in the rat.
Plasticity Following Injury
Plastic changes following damage to the brain are robust. Most CNS neurons attempt to regenerate but typically fail. This failure results in part from the actions of glial cells which show a marked plastic response to brain injury. For example, astrocytes, oligodendrocytes, and microglia rapidly proliferate at the site of injury. Astrocytes and oligodendrocytes both release proteoglycans that inhibit axon regeneration. Activated microglia provide a permissive environment. They release neurotrophins. However, their actions cannot overcome the inhibitory effects provided by the other cells.
Many neuroscientists draw a parallel between mechanisms of recovery of function following injury and the plasticity associated with learning and memory. For example, a now classic study by Raisman and Field examined the synaptic contacts onto septal neurons. Septal neurons receive afferent information from the fimbria and medial forebrain bundle. These inputs make approximately equal numbers of synaptic contacts onto septal neurons. In their experiment, Raisman and Field lesioned one or the other of the inputs and counted synapses over a period of time. They found that, within 1 or 2 days of the lesion, synaptic contacts onto the septal neurons decreased by about 50% (commensurate with axon degeneration of the cut pathway). But, over the course of several weeks, the synaptic numbers once again approached normal levels. They determined that the new synaptic contacts were coming from the pathway that was not lesioned. In other words, neurons from the intact path were sprouting axonal branches and making additional synaptic contact with the septal neurons. This process is known as collateral sprouting. This was a landmark study in that it was the first to demonstrate that nondamaged areas of the brain try to compensate for damage.
More recently, this idea of compensation has been examined in the somatosensory cerebral cortex. Michael Merzenich and his group have carefully mapped the topography of the hand onto the somatosensory cortex. In one study, they either lesioned a sensory nerve of one of the fingers or removed the finger and recorded the neural activity from the cortex. They expected to see diminished activity in the region of the cortex that had just lost its input from the finger. Instead, they found that the cortex displayed neural responses to stimulation of parts of the hand adjacent to the damaged nerve or removed finger. This observation is consistent with the idea that adjacent portions of the body make synapses in their own area of the cortex as well as adjacent portions, but that the synapses that are formed in adjacent areas are repressed. When the finger information is removed, a short-term plastic change occurs that removes the repression associated with synapses from the adjacent parts of the cortex. In other words, the motor maps for adjacent portions of the body have expanded or taken over the functions of the denervated cortex. Further, Merzenich’s group reports that over the course of a month or two, axons in adjacent regions of the cortex sprout collaterals that will more fully innervate the denervated region. The consequence of this is that adjacent body parts become more sensitive to stimulation.
Subsequent studies have indicated that the plasticity associated with collateral sprouting follows Hebbian rules; that is, synaptic formation and strengthening are dependent on correlated activity in preand postsynaptic neurons. Further, this mechanism appears to be dependent on activation of the NMDA receptor and calcium influx.
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