• 제목/요약/키워드: Neuronal Plasticity

검색결과 81건 처리시간 0.032초

Phytochemicals That Act on Synaptic Plasticity as Potential Prophylaxis against Stress-Induced Depressive Disorder

  • Soojung, Yoon;Hamid, Iqbal;Sun Mi, Kim;Mirim, Jin
    • Biomolecules & Therapeutics
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    • 제31권2호
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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.

뇌유래신경영양인자와 뇌 신경가소성: 비약물적 개입 (Brain-Derived Neurotrophic Factor and Brain Plasticity: Non-Pharmacological Intervention)

  • 김낙영;임현국
    • 생물정신의학
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    • 제30권1호
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    • pp.1-6
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    • 2023
  • Many psychiatric disorders are associated with brain functional dysfunctions and neuronal degeneration. According to the research so far, enhanced brain plasticity reduces neurodegeneration and recovers neuronal damage. Brain-derived neurotrophic factor (BDNF) is one of the most extensively studied neurotrophins in the mammalian brain that plays major roles in neuronal survival, development, growth, and maintenance of neurons in brain circuits related to emotion and cognitive function. Also, BDNF plays an important role in brain plasticity, influencing dendritic spines in the hippocampus neurogenesis. Changes in neurogenesis and dendritic density can improve psychiatric symptoms and cognitive functions. BDNF has potent effects on brain plasticity through biochemical mechanisms, cellular signal pathways, and epigenetic changes. There are pharmacological and non-pharmacological interventions to increase the expression of BDNF and enhance brain plasticity. Non-pharmacological interventions such as physical exercise, nutritional change, environmental enrichment, and neuromodulation have biological mechanisms that increase the expression of BDNF and brain plasticity. Non-pharmacological interventions are cost-effective and safe ways to improve psychiatric symptoms.

Neuronal Activity-Dependent Regulation of MicroRNAs

  • Sim, Su-Eon;Bakes, Joseph;Kaang, Bong-Kiun
    • Molecules and Cells
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    • 제37권7호
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    • pp.511-517
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    • 2014
  • MicroRNAs are non-coding short (~23 nucleotides) RNAs that mediate post-transcriptional regulation through sequence-specific gene silencing. The role of miRNAs in neuronal development, synapse formation and synaptic plasticity has been highlighted. However, the role of neuronal activity on miRNA regulation has been less focused. Neuronal activity-dependent regulation of miRNA may finetune gene expression in response to synaptic plasticity and memory formation. Here, we provide an overview of miRNA regulation by neuronal activity including high-throughput screening studies. We also discuss the possible molecular mechanisms of activity-dependent induction and turnover of miRNAs.

Physical Activity and Brain Plasticity

  • Moon, Hyo Youl;van Praag, Henriette
    • 운동영양학회지
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    • 제23권4호
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    • pp.23-25
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    • 2019
  • Recent research suggests that the brain has capable of remarkable plasticity and physical activity can enhance it. In this editorial letter, we summarize the role of hippocampal plasticity in brain functions. Furthermore, we briefly sketched the factors and mechanisms of motion that influence brain plasticity. We conclude that physical activity can be an encouraging intervention for brain restoration through neuronal plasticity. At the same time, we suggest that a mechanistic understanding of the beneficial effects of exercise should be accompanied in future studies.

A Simple Method for Predicting Hippocampal Neurodegeneration in a Mouse Model of Transient Global Forebrain Ischemia

  • Cho, Kyung-Ok;Kim, Seul-Ki;Cho, Young-Jin;Sung, Ki-Wug;Kim, Seong Yun
    • The Korean Journal of Physiology and Pharmacology
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    • 제10권4호
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    • pp.167-172
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    • 2006
  • In the present study, we developed a simple method to predict the neuronal cell death in the mouse hippocampus and striatum following transient global forebrain ischemia by evaluating both cerebral blood flow and the plasticity of the posterior communicating artery (PcomA). Male C57BL/6 mice were anesthetized with halothane and subjected to bilateral occlusion of the common carotid artery (BCCAO) for 30 min. The regional cerebral blood flow (rCBF) was measured by laser Doppler flowmetry. The plasticity of PcomA was visualized by intravascular perfusion of India ink solution. When animals had the residual cortical microperfusion less than 15% as well as the smaller PcomA whose diameter was less than one third compared with that of basilar artery, neuronal damage in the hippocampal subfields including CA1, CA2, and CA4, and in the striatum was consistently observed. Especially, when mice met these two criteria, marked neuronal damage was observed in CA2 subfield of the hippocampus. In contrast, after transient BCCAO, neuronal damage was consistently produced in the striatum, dependent more on the degree of rCBF reduction than on the plasticity of PcomA. The present study provided simple and highly reproducible criteria to induce the neuronal cell death in the vulnerable mice brain areas including the hippocampus and striatum after transient global forebrain ischemia.

정신치료의 신경생물학적 기전 (Neurobiological Mechanism of Psychotherapy)

  • 이승환;김승현
    • 생물정신의학
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    • 제9권2호
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    • pp.79-94
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    • 2002
  • Polarisation of biological and psychosocial aspects of psychiatry is nowadays main stream. Current knowledges of the interaction between biology and psychology make it possible to consider a truly integrative approach of the two aspects. Research findings suggest that the neuronal plasticity is the key mechanism to answer how the mental function work to an environmental stimuli and how the psychotherapeutic approach work on the brain. Advances in neuroscience research have led to a more sophisticated understanding of how psychotherapy may affect brain function. Even though there have been a tremendous efforts to find out the neurobiological mechanism of mental function, the answer is at best premature. In this article, research findings about of neuronal plasticity, implicit memory, animal studies which were associated with psychotherapy and psychological aspects were reviewed.

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Unsuspected Plasticity of Single Neurons after Connection of the Corticospinal Tract with Peripheral Nerves in Spinal Cord Lesions

  • Brunelli, Giorgio;Wild, Klaus von
    • Journal of Korean Neurosurgical Society
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    • 제46권1호
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    • pp.1-4
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    • 2009
  • Objective: To report an unsuspected adaptive plasticity of single upper motor neurons and of primary motor cortex found after microsurgical connection of the spinal cord with peripheral nerve via grafts in paraplegics and focussed discussion of the reviewed literature. Methods: The research aimed at making paraplegics walk again, after 20 years of experimental surgery in animals. Amongst other things, animal experiments demonstrated the alteration of the motor endplates receptors from cholinergic to glutamatergic induced by connection with upper motor neurons. The same paradigm was successfully performed in paraplegic humans. The nerve grafts were put into the ventral-lateral spinal tract randomly, with out possibility of choosing the axons coming from different areas of the motor cortex. Results: The patient became able to selectively activate the re-innervated muscles she wanted without concurrent activities of other muscles connected with the same cortical areas. Conclusion: Authors believe that unlike in nerve or tendon transfers, where the whole cortical area corresponding to the transfer changes its function a phenomenon that we call "brain plasticity by areas". in our paradigm due to the direct connection of upper motor neurons with different peripheral nerves and muscles via nerve grafts motor learning occurs based on adaptive neuronal plasticity so that simultaneous contractions of other muscles are prevented. We propose to call it adaptive functional "plasticity by single neurons". We speculate that this phenomenon is due to the simultaneous activation of neurons spread in different cortical areas for a given specific movement, whilst the other neurons of the same areas connected with peripheral nerves of different muscles are not activated at the same time. Why different neurons of the same area fire at different times according to different voluntary demands remains to be discovered. We are committed to solve this enigma hereafter.

Reconstruction of Neural Circuits Using Serial Block-Face Scanning Electron Microscopy

  • Kim, Gyu Hyun;Lee, Sang-Hoon;Lee, Kea Joo
    • Applied Microscopy
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    • 제46권2호
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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.

Memory allocation at the neuronal and synaptic levels

  • HyoJin Park;Bong-Kiun Kaang
    • BMB Reports
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    • 제57권4호
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    • pp.176-181
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    • 2024
  • Memory allocation, which determines where memories are stored in specific neurons or synapses, has consistently been demonstrated to occur via specific mechanisms. Neuronal allocation studies have focused on the activated population of neurons and have shown that increased excitability via cAMP response element-binding protein (CREB) induces a bias toward memory-encoding neurons. Synaptic allocation suggests that synaptic tagging enables memory to be mediated through different synaptic strengthening mechanisms, even within a single neuron. In this review, we summarize the fundamental concepts of memory allocation at the neuronal and synaptic levels and discuss their potential interrelationships.