Cerebral Plasticity

What is cerebral plasticity…?

                        Cerebral  plasticity  refers to the ability of the brain  and  nervous system in all species to change structurally and functionally as a result of input from the environment.

Learning  is the ability to acquire new information or skills through instruction or experience.Memory is the process by which information acquired through learning is stored and retreived.For an experience to become part of memory , it must produce persistent structural and functional changes that represent the experience in the brain.This capability for change associated with learning is termed as  plasticity.

Nervous system plasticity underlies our ability to change our behavior in response to stimuli from the external and internal  environments. It involves changes in individual neurons as well as changes in the strengths of synaptic connections among neurons. The capacity to change is a fundamental characteristic of nervous systems When the nervous system changes, there is often a correlated change in behavior or psychological function. This behavioral change is known by names such as learning, memory, addiction, maturation, and recovery. Thus, for example, when people learn new motor skills, such as in playing a musical instrument, there are plastic changes in the structure of cells in the nervous system that underlie the motor skills. If the plastic changes are somehow prevented from occurring, the motor learning does not occur.

To illustrate plasticity, imagine making an impression of a coin in a lump of clay. In order for the impression of the coin to appear in the clay, changes must occur in the clay -- the shape of the clay changes as the coin is pressed into the clay. Similarly, the neural circuitry in the brain must reorganize in response to experience or sensory stimulation.

Facts about neural plasticity

FACT 1:

• Neuroplasticity includes several different processes that take place throughout a lifetime.
• Neuroplasticity does not consist of a single type of morphological change, but rather includes several different processes that occur throughout an individual’s lifetime.

FACT 2:

• Neuroplasticity has a clear age-dependent determinant.
• Although plasticity occurs over an individuals lifetime, different types of plasticity dominate during certain periods of ones life and are less prevalent during other periods.

FACT 3:

• Neuroplasticity occurs in the brain under two primary conditions:
• 1. During normal brain development when the immature brain first begins to process sensory information through adulthood .
• 2. As an adaptive mechanism to compensate for lost function and/or to maximize remaining functions in the event of brain injury.

FACT 4

• The environment plays a key role in influencing plasticity.
• In addition to genetic factors, the brain is shaped by the characteristics of a person's environment and by the actions of that same person.
• Plasticity occurs on a variety of levels, ranging from cellular changes involved in learning, to large-scale changes involved in cortical remapping in response to injury.

                                                         The most widely recognized forms of plasticity are learning, memory, and recovery from brain damage.

During most of the 20th century, the general consensus among neuroscientists was that brain structure is relatively immutable after a critical period during early childhood. This belief has been challenged by new findings, revealing that many aspects of the brain remain plastic even into adulthood

Neuroplasticity can work in two directions; it is responsible for deleting old connections as frequently as it enables the creation of new ones. Through this process, called “synaptic pruning,” connections that are inefficient or infrequently used are allowed to fade away, while neurons that are highly routed with information will be preserved, strengthened, made even more synaptically dense..Closely tied in with the pruning process, then, is our ability to learn and to remember. While each neuron acts independently, learning new skills may require large collections of neurons to be active simultaneously to process neural information; the more neurons activated, the better we learn.

SYNAPTIC PRUNING

Synaptic pruning, neuronal pruning or neuro-structural re-assembly refer to neurological regulatory processes, which facilitate a change in neural structure by reducing the overall number of neurons or connections, leaving more efficient synaptic configurations. The purpose of synaptic pruning is believed to be to remove unnecessary neuronal structures from the brain; as the human brain develops, the need to understand more complex structures becomes much more pertinent, and simpler associations formed at childhood are thought to be replaced by complex structures .Synaptic pruning eliminates weaker synaptic contacts while stronger connections are kept and strengthened. Experience determines which connections will be strengthened and which will be pruned; connections that have been activated most frequently are preserved.Neurons must have a purpose to survive. Neurons without a purpose , die through a process called apoptosis  in which neurons that do not receive or transmit information become damaged and die. Ineffective or weak connections are "pruned" in much the same way a gardener would prune a tree or bush, giving the plant the desired shape. It is plasticity that enables the process of developing and pruning connections, allowing the brain to adapt itself to its environment.

• Hebb’s theory  (Donald Hebb in 1949.)

Hebbian theory describes a basic mechanism for synaptic plasticity wherein an increase in synaptic efficacy arises from the  presynaptic cell's  repeated and  persistent  stimulation of the postsynaptic cell. it is also called Hebb's rule, Hebb's postulate, and cell assembly theory .The theory is often summarized as "Cells that fire together, wire together.“ It attempts to explain "associative learning", in which simultaneous activation of cells leads to pronounced increases in synaptic strength between those cells. Such learning is known as Hebbian learning.

Plasticity of Learning and Memory

According to Durbach (2000), there appear to be at least two types of modifications that occur in the brain with learning:

• A change in the internal structure of the neurons, the most notable being in the area of synapses.
• An increase in the number of synapses between neurons.

                                      Initially, newly learned data are "stored" in short-term memory, which is a temporary ability to recall a few pieces of information. Some evidence supports the concept that short-term memory depends upon electrical and chemical events in the brain as opposed to structural changes such as the formation of new synapses. One theory of short-term memory states that memories may be caused by  reverberating neuronal circuits -- that is, an incoming nerve impulse stimulates the first neuron which stimulates the second, and so on, with branches from the second neuron synapsing with the first. After a period of time, information may be moved into a more permanent type of memory, long-term memory, which is the result of anatomical or biochemical changes that occur in the brain (Tortora and Grabowski, 1996).

THE DAMAGED BRAIN- CAN NEUROPLASTICITY HELP?

Neuroplasticity is the saving grace of the damaged or disabled brain; without it, lost functions could never be regained, nor could disabled processes ever hope to be improved. Plasticity allows the brain to rebuild the connections that, because of trauma, disease, or genetic misfortune, have resulted in decreased abilities. It also allows us to compensate for irreparably damaged or dysfunctional neural pathways by strengthening or rerouting our remaining ones. While these processes are likely to occur in any number of ways, scientists have identified four major patterns of plasticity that seem to work best in different situations.

•  The process, called “functional map expansion,” results in changes to the amount of brain surface area dedicated to sending and receiving signals from some specific part of the body. 
•  For example, the case in which healthy cells surrounding an injured area of the brain change their function, even their shape, so as to compensate for the functions executed by neurons at the site of injury.
• Brain cells can also reorganize existing synaptic pathways; this form of plasticity, known as a “compensatory masquerade”  ,  allows already-constructed pathways that neighbor a damaged area to respond to changes in the body’s demands caused by lost function in some other area. 
• another neuroplastic process, “homologous region adoption,”  allows one entire brain area to take over functions from another distant brain area (one not immediately neighboring the compensatory area) that has been damaged. 
• finally, neuroplasticity can occur in the form of “cross model reassignment,” which allows one type of sensory input to entirely replace another damaged one.
• Cross-model reassignment allows the brain of a blind individual, in learning to read Braille, to rewire the sense of touch so that it replaces the responsibilities of vision in the brain areas linked with reading.`

FACTORS AFFECTING BRAIN PLASTICITY

•  experience (both pre- and postnatal)
•  psychoactive drugs
•  gonadal hormones (e.g., estrogen, testosterone)
• anti-inflammatory agents

•  growth factors (e.g., nerve growth factor)
•  dietary factors
•    genetic factors
•  stress
•  brain injury and disease

Early experience

                              It is generally assumed that experiences early in life have different effects on behavior than similar experiences later in life. The reason for this difference is not understood To investigate this question, Kolb, Gibb, & Gorny, 2003;    placed animals in complex environments either as juveniles, in adulthood, or in senescence.They  expected that there would be quantitative differences in the effects of experience on synaptic organization,  but they also found qualitative differences. They found that the length of dendrites and the density of synapses were increased in neurons in the motor and sensory cortical regions in adult and aged animals housed in a complex environment (relative to a standard lab cage).In contrast, animals placed in the same environment as juveniles showed an increase in dendritic length but a decrease in spine density.  In other words, the same environmental manipulation had qualitatively different effects on the organization of neuronal circuitry in juveniles than in adults.

• Kolb, Gibb, & Gorny, 2003;

                   The offspring of a rat housed in a complex environment during the term of her pregnancy have increased synaptic space on neurons in the cerebral cortex in adulthood.Although we do not know how prenatal experiences alter the brain, it seems likely that some chemical response by the mother, be it hormonal or otherwise, can cross the placental barrier and alter the genetic signals in the developing brain.        

§  Psychoactive drugs

                                         One experimental demonstration of a very persistent form of drug experience-dependent plasticity is known as behavioral sensitization.For example, if a rat is given a small dose of amphetamine, it initially will show a small increase in motor activity (e.g., locomotion, rearing). When the rat is given the same dose on subsequent occasions, however, the increase in motor activity increases, or sensitizes, and the animal may remain sensitized for weeks, months, or even years, even if drug treatment is discontinued.

• Robinson & Kolb, 1999

                                         A comparison of the effects of amphetamine and saline treatments on the structure of neurons in a brain region known as the nucleus accumbens, which mediates the psychomotor activating effects of amphetamine, showed that neurons in the amphetamine-treated brains had greater dendritic material, as well as more densely organized spines . Later studies have shown that these drug-induced changes are found not only when animals are given injections by an experimenter, but also when animals are trained to self-administer drugs, leading us to speculate that similar changes in synaptic organization be found in human drug addicts.

§  Brain injury and diseases

• Kolb, 1995

                                                      Brain injury disrupts the synaptic organization of the brain, and when there is functional improvement after the injury, there is a correlated reorganization of neural circuits .

•  Raldolph Nudo, (2003)

                                                    Functional and structural changes take place in the cerebral cortex after injury, such as occurs after stroke or trauma.  After cortical injury, the structure and function of undamaged parts of the brain are remodeled during recovery, shaped by the sensorimotor experiences of the individual in the weeks to months following injury.

§  Dietery factors

                                                        A diet, similar in composition to the typical diet of most industrialized western societies rich in saturated fat and refined sugar (HFS), can influence brain structure and function via regulation of neurotrophins.

     (Molteni, R.J Barnard, Z Ying^a, C.K Roberts, F Gómez-Pinilla   (2011)

§  stress

                                         One of the most important sources of stress in the wild is predator attack. In the human society context, predator attack has been replaced by different forms of traumatic experiences, including traffic accidents, wars, terrorist attacks, male violence against children and women, and sexual abuse. All these forms of stress may have permanent psychological consequences and lasting changes in  affect.In more severe cases, serious alterations may appear in the individuals that have suffered the stress, then the situation is recognized as posttraumatic stress disorder. Traumatic stress may result in plastic remodeling of certain brain regions, such as the amygdala.Brain imaging studies reveal a hyperexcitability of the right amygdala in the brain of humans exposed to traumatic situations (Rauch and Shin, 1997; Rauch et al., 1997; Shin et al., 2006). The amygdala also shows plastic changes in animals exposed to a fear conditioning paradigm.Fear conditioning is a form of associative Pavlovian learning in which the animals are exposed  to a stressful situation, such as en electric shock, that is associated with a sensory stimulus. In this paradigm, the animals learn to associate the sensory stimulus with the traumaticexperience. Thus, after learning the association, the sensory stimulus per se may switch on the fear response. Plastic synaptic changes in the amygdala underlie both acquisition and extinction of the enhanced fear response. Fear conditioning induces long-term potentiation of synaptic inputs to the amygdala, and several data support the view that fear conditioning is mediated by changes in synaptic strength at sensory inputs to the lateral nucleus of the amygdala

 (Blair et al., 2001; Maren, 2005; Maren et al., 1994; Rogan et al., 1997; Schafe et al., 2001; Sigurdsson et al., 2006).

§  Hormones

                                        Hormonal signals carry information from the body to the brain and regulate  brain plasticity. Hormonally regulated brain plastic modifications may then impact feelings, emotions, cognition, and behavior. In turn, feelings, emotions, cognitive changes, and behavioral responses modulate hormonal  levels by affecting brain plasticity.

     (García-Segura, Luis Miguel,(2009)

•  Gonadal steroids participate in the shaping of the developing brain, while their actions during adult life are implicated in higher brain functions such as cognition, mood and memory.
•   Gonadal steroid-induced functional changes are accompanied by alterations in neuron and synapse numbers, as well as in dendritic and synaptic morphology. These structural modifications serve as a morphological basis for changes in behavior and cellular activity. (Hoyk and Leranth, 2006.