NEUROPLASTICITY : PLASTICITY IN BRAIN

 ABSTRACT

Research in the field of neurosciences and genetics has given us great insight into the understanding of learning, behavior and changes in the brain in response to experience. It is seen that brain is dynamically changing throughout life and is capable of tearing at any time. Plastic reorganization of the brain is now being studied in children and adults with new noninvasive tools such as functional brain magnetic resonance imaging.  Increasing evidence demonstrates that neuroplasticity, a fundamental mechanism of neuronal adaptation, is disrupted in mood disorders. Here we provide an overview of the evidence that chronic stress, which can precipitate or exacerbate depression, disrupts neuroplasticity, while antidepressant treatment produces opposing effects and can enhance neuroplasticity. Promising therapies that may enhance training-induced cognitive and motor learning, such as brain stimulation and neuropharmacological interventions, were identified, along with questions of how best to use this body of information to reduce human disability. Improved understanding of adaptive mechanisms at every level, from molecules to synapses, to networks, to behaviour, can be gained from iterative collaborations between basic and clinical researchers. Improved means of assessing neuroplasticity in humans, including biomarkers for predicting and monitoring treatment response, are needed. Neuroplasticity occurs with many variations, in many forms, and in many contexts. However, common themes in plasticity that emerge across diverse central nervous system conditions include experience dependence, time sensitivity and the importance of motivation and attention. Integration of information across disciplines should enhance opportunities for the translation of neuroplasticity and circuit retraining research into effective clinical therapies. Understanding how the brain's circuitry is sculpted during development provides an important perspective for thinking about neurodevelopmental disorders.

Keywords: neuroplasticity, plastic, remodel, neuropharmacological  interventions

INTRODUCTION

Neuroplasticity refers to the inherently dynamic biological capacity of the central nervous system (CNS) to undergo maturation, change structurally and functionally in response to experience and to adapt following injury. 

 The term “neuronal plasticity” was already used by the “father of neuroscience” Santiago Ramón y Cajal (1852-1934) who described non-pathological changes in the structure of adult brains. In a wider sense, plasticity of the brain can be regarded as “the ability to make adaptive changes related to the structure and function of the nervous system”. Accordingly, “neuronal plasticity” can stand not only for morphological changes in brain areas, for alterations in neuronal networks including changes in neuronal connectivity as well as the generation of new neurons (neurogenesis), but also for neurobiochemical changes.

MECHANISMS FOR PLASTICITY IN THE CENTRAL NERVOUS SYSTEM

Several mechanisms that involve neuronal plasticity stand out as important contributors to the developing brain’s ability to acquire new information, change in response to environmental stimulation, and recover from injury. 

The processes that control neurogenesis and cell death by apoptosis are carefully controlled in fetal life to assure that proper number of neurons take their places in each region of the brain during the second trimester. 

Studies in animals indicate that there is a marked overproduction of neurons in the fetus when compared with the final number in the mature brain, and that the final complement is determined by programmed cell death as well as by the programs for neurogenesis. Mice with mutations in genes for caspase enzymes involved in apoptosis have reduced cell death in fetal life and develop an expanded cerebral cortex that is too large for the skull.

 Overproduction of neurons could be adaptive for the brain by creating a reservoir that is available to repair injury in the fetus.Recent evidence indicates that neurogenesis persists beyond the fetal period and into adulthood in certain areas of the brain including the subventricular zone of the lateral ventricles and the subgranular zone of the dentate gyrus of the hippocampus. In neonatal rats with experimental hypoxic-ischemic injury, sustained neurogenesis persists in the subventricular zone for months after injury and continues to populate the cerebral cortex with new neurons. A similar phenomenon has been shown to occur in adult rodents after stroke. Newborn neurons integrate into existing circuits and could contribute to recovery from injury. In addition to their potential role in replacing damaged neurons, newborn stem cells have been shown to have a protective effect when injected within days after injury, possibly by expressing growth factors.

ACTIVITY-DEPENDENT NEURONAL PLASTICITY

In addition to modulation of neurogenesis, changes in the strength of synapses and reorganization of neuronal circuits also play important roles in brain plasticity. Synaptic plasticity refers to changes in the strength of neurotransmission induced by activity experienced by the synapse in the past. Changes in the frequency or strength of activation across synapses can result in long-term increases or decreases in their strength, referred to as either long-term potentiation (LTP) or long-term depression (LTD), respectively. These activity dependent changes occur in all excitatory synapses that use glutamate as their neurotransmitter as well as in some inhibitory GABAergic synapses. They can be mediated by changes in the release of neurotransmitter from presynaptic terminals as well as changes in the number of excitatory receptors on postsynaptic neurons. 

LTP can be produced experimentally by rapid repetitive presynaptic stimulation of synapses on pyramidal neurons in the CA1 region of the hippocampus and this is the best studied form of synaptic plasticity. Rapid stimulation of synapses opens NMDA-type glutamate receptors in the postsynaptic membrane leading to an increase in intracellular calcium and insertion of AMPA type glutamate receptors in the postsynaptic membrane.

AMPA receptors move into the postsynaptic membrane from a receptor pool located in endosomes within the cytoplasm of dendritic spines through a process called receptor trafficking. Activation of signaling cascades, including calcium calmodulin II (CaMKII), by calcium fluxed through NMDA channels plays an essential role in this process. Release of the neuronal growth factor brain-derived neuronal growth factor (BDNF) from electrically active neurons enhances the formation of LTP, and this process is associated with an enlargement of dendritic spines. LTP is enhanced in the immature brain as compared to the adult brain. In contrast to LTP, LTD is produced by slow repetitive stimulation of excitatory synapses and is related to a reduction in AMPA receptors in the postsynaptic membrane as they move into the cytoplasm into endosomes. Another form of LTD is caused by the stimulation of type I metabotropic glutamate receptors that activate phosphoinositide turnover in dendritic spines. This form of plasticity is prominent in the cerebellum. LTP is associated with memory formation in the hippocampus, and LTP and LTD form the basis for activity-dependent reorganization and stabilization of developing neuronal networks in sensory motor cortex. Prolonged in vivo imaging of neurons in rodent cerebral cortex indicates that sensory experience drives the continuous sprouting and retraction of synapses located on dendritic spines to remodel neural circuits. Similar mechanisms are probably responsible for enhanced excitability in cerebral cortex that has been documented following short periods of motor skill training using the hands or lower legs.

CONCLUSION

Therefore neuroplasticity is remodel and reorganize for purpose of better ability to adapt to new situations. Despite the fact that the concept of neuroplasticity is quite new, it is one of the most important discoveries in neuroscience. The fact is that neural networks are not fixed, but occurring and disappearing dynamically throughout our whole life, depending on experiences. While we repeatedly practice one activity such as a sequence of movements or a mathematical problem, neuronal circuits are being formed, leading to better ability to perform the practiced task with less waste of energy.