• PNF and Movement
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• v.6 no.2
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• pp.31-38
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• 2008

Purpose: The purpose of this study were to overview the effect of exercise on neural plasticity and the proteins related to neural plasticity. Results: Exercise increased levels of BDNF(brain-derived neurotrophic factor), Insulin-like growth factor-I (IGF-I), Synapsin, Synaptophysin, VEGF(vascular endothelial growth factor) and other growth factors, stimulate neurogenesis, increase resistance to brain insult and improve learning and mental performance. These proteins improved synaptic plasticity by directly affecting synaptic structure and potentiating synaptic strength, and by strengthening the underlying systems that support plasticity including neurogenesis, metabolism and vascular function. Conclusion: Exercise-induced structural and functional change by these proteins can effect on functional movement, cognition in healthy and brain injured people and animals.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.1
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• pp.1-8
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• 2016

Damage in the periphery or spinal cord induces maladaptive plastic changes along the somatosensory nervous system from the periphery to the cortex, often leading to chronic pain. Although the role of neural circuit remodeling and structural synaptic plasticity in the 'pain matrix' cortices in chronic pain has been thought as a secondary epiphenomenon to altered nociceptive signaling in the spinal cord, progress in whole brain imaging studies on human patients and animal models has suggested a possibility that plastic changes in cortical neural circuits may actively contribute to chronic pain symptoms. Furthermore, recent development in two-photon microscopy and fluorescence labeling techniques have enabled us to longitudinally trace the structural and functional changes in local circuits, single neurons and even individual synapses in the brain of living animals. These technical advances has started to reveal that cortical structural remodeling following tissue or nerve damage could rapidly occur within days, which are temporally correlated with functional plasticity of cortical circuits as well as the development and maintenance of chronic pain behavior, thereby modifying the previous concept that it takes much longer periods (e.g. months or years). In this review, we discuss the relation of neural circuit plasticity in the 'pain matrix' cortices, such as the anterior cingulate cortex, prefrontal cortex and primary somatosensory cortex, with chronic pain. We also introduce how to apply long-term in vivo two-photon imaging approaches for the study of pathophysiological mechanisms of chronic pain.

• Journal of Korean Physical Therapy Science
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• v.1 no.2
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• pp.301-311
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• 1994

Most patients treated by physical therapists have suffered some neurological trauma resulting from disease or injury. The traditional teaching used to be that damage of central neurons is irreversible. However, it has been necessary to cast aside this traditional view because of accumulating evidence that the brain is endowed with remarkable plasticity. This paper reviews the literature relating to neuroplasticity within the brain and draws implications pertinent to physical therapy practice.

• Proceedings of the Korean Society for Technology of Plasticity Conference
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• 1994.10a
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• pp.133-140
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• 1994

In this paper, we have proposed a new method to determine the initial billet for the forged products using a function approximation in neural networks. the architecture of neural network is a three-layer neural network and the back propagation algorithm is employed to train the network. By utilizing the ability of function approximation of neural network, an optimal billet is determined by applying nonlinear mathematical relationship between shape ratio in the initial billet and the final products. A volume of incomplete filling in the die is measured by the rigid-plastic finite element method. The neural network is trained with the initial billet shape ratio and that of the un-filled volume. After learning, the system is able to predict the filling region which are exactly the same or slightly different to results of finite element method. It is found that the prediction of the filling shape ratio region can be made successfully and the finite element method results are represented better by the neural network.

• Korean Journal of Biological Psychiatry
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• v.8 no.1
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• pp.3-19
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• 2001

Recent basic and clinical studies demonstrate a major role for neural plasticity in the etiology and treatment of depression and stress-related illness. The neural plasticity is reflected both in the birth of new cell in the adult brain(neurogenesis) and the death of genetically healthy cells(apoptosis) in the response to the individual's interaction with the environment. The neural plasticity includes adaptations of intracellular signal transduction pathway and gene expression, as well as alterations in neuronal morphology and cell survival. At the cellular level, repeated stress causes shortening and debranching of dendrite in the CA3 region of hippocampus and suppress neurogenesis of dentate gyrus granule neurons. At the molecular level, both form of structural remodeling appear to be mediated by glucocorticoid hormone working in concert with glutamate and N-methyl-D-aspartate(NMDA) receptor, along with transmitters such as serotonin and GABA-benzodiazepine system. In addition, the decreased expression and reduced level of brain-derived neurotrophic factor(BDNF) could contribute the atrophy and decreased function of stress-vulnerable hippocampal neurons. It is also suggested that atrophy and death of neurons in the hippocampus, as well as prefrontal cortex and possibly other regions, could contribute to the pathophysiology of depression. Antidepressant treatment could oppose these adverse cellular effects, which may be regarded as a loss of neural plasticity, by blocking or reversing the atrophy of hippocampal neurons and by increasing cell survival and function via up-regulation of cyclic adenosine monophosphate response element-binding proteins(CREB) and BDNF. In this article, the molecular and cellular mechanisms that underlie stress, depression, and action of antidepressant are precisely discussed.

• The Journal of Korean Physical Therapy
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• v.13 no.3
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• pp.791-797
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• 2001

After brain injury, patients show a wide range in the degree of recovery. By a variety of mechanisms, the human brain is constantly undergoing plastic changes. Spontaneous recovery from brain injury in the chronic stage omes about because of plasticity. The brain regions are altered. resulting in functionally modified cortical network. This review cnsidered the neural plasticity from cellular and molecular mechanisms of synapse formation to behavioural recovery from brain injury in elderly humans. The stimuli required to elicit plasticity are thought to be activity-dependent elements. especially exercise and learning. Knowledge about the physiology of brain plasticity has led to the development of methods for rehabilitation.

• Proceedings of the Korean Society for Technology of Plasticity Conference
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• 2000.04a
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• pp.71-74
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• 2000

The equi-potential lines designed in the electric field are introduced to find the preform shape in axisymmetric hot forging. The equi-potential lines generated between two conductors of different voltages show similar trends of the minimum work paths between the undeformed shape and the deformed shape. Base on this similarity the equi-potential lines obtained by arrangement of the initial and final shapes are utilized for the design of preform and then the artificial neural network is used to find the range of initial volume and potential value of the electric field.

• Applied Microscopy
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• v.46 no.2
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• pp.100-104
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• 2016

Electron microscopy is currently the only available technique with a spatial resolution sufficient to identify fine neuronal processes and synaptic structures in densely packed neuropil. For large-scale volume reconstruction of neuronal connectivity, serial block-face scanning electron microscopy allows us to acquire thousands of serial images in an automated fashion and reconstruct neural circuits faster by reducing the alignment task. Here we introduce the whole reconstruction procedure of synaptic network in the rat hippocampal CA1 area and discuss technical issues to be resolved for improving image quality and segmentation. Compared to the serial section transmission electron microscopy, serial block-face scanning electron microscopy produced much reliable three-dimensional data sets and accelerated reconstruction by reducing the need of alignment and distortion adjustment. This approach will generate invaluable information on organizational features of our connectomes as well as diverse neurological disorders caused by synaptic impairments.

• Applied Microscopy
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• v.46 no.4
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• pp.171-175
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• 2016

A distinctive neuronal network in the brain is believed to make us unique individuals. Electron microscopy is a valuable tool for examining ultrastructural characteristics of neurons, synapses, and subcellular organelles. A recent technological breakthrough in volume electron microscopy allows large-scale circuit reconstruction of the nervous system with unprecedented detail. Serial-section electron microscopy-previously the domain of specialists-became automated with the advent of innovative systems such as the focused ion beam and serial block-face scanning electron microscopes and the automated tape-collecting ultramicrotome. Further advances in microscopic design and instrumentation are also available, which allow the reconstruction of unprecedentedly large volumes of brain tissue at high speed. The recent introduction of correlative light and electron microscopy will help to identify specific neural circuits associated with behavioral characteristics and revolutionize our understanding of how the brain works.

• Biomolecules & Therapeutics
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• v.31 no.2
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• pp.148-160
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• 2023

Depression is a neuropsychiatric disorder associated with persistent stress and disruption of neuronal function. Persistent stress causes neuronal atrophy, including loss of synapses and reduced size of the hippocampus and prefrontal cortex. These alterations are associated with neural dysfunction, including mood disturbances, cognitive impairment, and behavioral changes. Synaptic plasticity is the fundamental function of neural networks in response to various stimuli and acts by reorganizing neuronal structure, function, and connections from the molecular to the behavioral level. In this review, we describe the alterations in synaptic plasticity as underlying pathological mechanisms for depression in animal models and humans. We further elaborate on the significance of phytochemicals as bioactive agents that can positively modulate stress-induced, aberrant synaptic activity. Bioactive agents, including flavonoids, terpenes, saponins, and lignans, have been reported to upregulate brain-derived neurotrophic factor expression and release, suppress neuronal loss, and activate the relevant signaling pathways, including TrkB, ERK, Akt, and mTOR pathways, resulting in increased spine maturation and synaptic numbers in the neuronal cells and in the brains of stressed animals. In clinical trials, phytochemical usage is regarded as safe and well-tolerated for suppressing stress-related parameters in patients with depression. Thus, intake of phytochemicals with safe and active effects on synaptic plasticity may be a strategy for preventing neuronal damage and alleviating depression in a stressful life.