• Molecules and Cells
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• v.37 no.7
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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.

• 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.

• BMB Reports
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• v.42 no.3
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• pp.131-135
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• 2009

MicroRNAs control gene expression by inhibiting translation or promoting degradation of their target mRNAs. Since the discovery of the first microRNAs, lin-4 and let-7, in C. elegans, hundreds of microRNAs have been identified as key regulators of cell fate determination, lifespan, and cancer in species ranging from plants to humans. However, while microRNAs have been shown to be particularly abundant in the brain, their role in the development and activity of the nervous system is still largely unknown. In this review, we describe recent advances in our understanding of microRNA function at synapses, the specialized structures required for communication between neurons and their targets. We also propose how these advances might inform the molecular model of memory.

• Proceedings of the Korean Institute of Information and Commucation Sciences Conference
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• 2001.05a
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• pp.325-328
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• 2001

정상적인 뉴런의 활성전위는 외부에서 일정한 자극이 인가되었을 때 세포막을 기준으로 하여 각 이온간의 농도 차에 의해 발생한다. 최근에 관심이 되어지고 있는 쇼크에 의한 세포가 손상이 발생할 경우, 즉 신호를 받아들이고 전달하는 뉴런 중에서 축색에 이온채널이 이상증세를 발생하면 신경 전달 흐름을 흐트러지게 하여 이웃한 정상세포에게 커다란 영향을 미치게 된다. 이것은 병리학적인 중요한 역할을 하는 축색 내에 이상이 발생하였다고 가정을 하지만 이 가정을 뒷받침 해 주는 증거는 매우 적다고 보고되고 있다. 최근 연구에서 손상된 축색의 모델은 쇼크이후에 이온의 칼륨 채널에 blocking 현상이 발생하여 나트륨 이온이 다수 유입됨을 고려하고있다. 이에 본 연구에서는 쇼크나 충격에 의해 축색의 손상을 입을 경우 운동신경의 변형으로부터 병리학적인 중요한 이상결과를 일으킬 수 있는 상태를 고려하여 신경모델을 설계해 시뮬레이션 해 보았다.

• 제어로봇시스템학회:학술대회논문집
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• 2000.10a
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• pp.516-516
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• 2000

We propose a neuron model that is possible to learn three-dimensional movement. The neuron model by imitating structure of a neuron, has the system resemble a neuron. We considered a neuron system based on the arguments, and wished to examine whether the system had reasonable function. Koch, Poggio and Torre believed that inhibition signal would shunt excitation signal on the dendrites. They believed that excitation signal operated input-signals and inhibition did as delayed ones. Thus, they were sure that function for directional selectivity was arisen by the shunting. Koch's concept is so important; therefore, we construct the neuron system with their concept. The neuron system makes the shunting function; thus, the model may have a function for directional selectivity. We initialized the connections and the dendrites by random data, and trained them by the back-propagation algorithm for three-dimensional movement. We made sure the defection of three-dimensional movement in the system.

• Toxicological Research
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• v.13 no.4
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• pp.417-421
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• 1997

Synaptobrevin is a kind of vesicle associated membrane proteins (VAMPs) which plays a secretary role in the neuronal synapse and was recently known as the biochemical target of botulinum neurotoxin type B. The structural gene of the synaptobrevin was cloned from mouse brain using RT-PCR technique and was seqrtenced. The deduced amino acid sequence showed that the synaptobrevin protein from mouse brain is exactly the same with that of the rat brain in the amino acid level. The synaptobrevin gene was subcloned into pET3a vector and expressed in E. coli. The molecular weight of the recombinant protein was 19 kDa as expected. Moreover, when the recombinant synaptobrevin protein was incubated with the native neurotoxin of Clostridium botulinum type B, it was cleaved by the toxin in a time dependent manner. This implies that the recombinant synaptobrevin protein and the native toxin are reacted in the same way as the native synaptobrevin did in the neuronal cells.

• 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.

• Journal of Sensor Science and Technology
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• v.27 no.1
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• pp.64-67
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• 2018

A new CMOS neuron circuit for implementing bistable synapses with spike-timing-dependent plasticity (STDP) properties has been proposed. In neuromorphic systems using STDP properties, the short-term dynamics of the synaptic efficacies are governed by the relative timing of the pre- and post-synaptic spikes, and the efficacies tend asymptotically to either a potentiated state or to a depressed one on long time scales. The proposed circuit consists of a negative shifter, a current starved inverter and a schmitt trigger designed using 0.18um CMOS technology. The simulation result shows that the proposed circuit can reduce the total size of neurons, and the spike energy of the proposed circuit is much less compared to the conventional circuits.

• The Zoological Society Korea : Newsletter
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• v.18 no.2
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• pp.12-20
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• 2001

2000년도 노벨 의학상은 스웨덴의 아비스 칼슨 박사 등 3명 이 수상했다. 그들은 신경전달 물질(neurotransmitter) 중 도파민 (dopamine)과 시냅스(synapse)에 관한 연구로 항 우울제 치료제인 프로작 (prozac)을 개발하여 신경, 정신질환 치료제 개발에 기여한 공로였다. 도파민과 GABA는 신경전달 물질 중의 하나로 도파민은 운동, 정서, 행동, 희노애락 등을 조절하는 것으로 이상 분비될 때 파킨스씨병, 정신분열증, 우울증 등을 유발시킨다. GABA는 억제성 신경전달물질로 이상 분비시 간질 등을 유발시킨다. 도파민과 GABA의 분비는 시냅스 후(postsynapse) 수용체에서 그 기능이 조절된다. 그러나 마약성인 코카인, 헤로인, 몰핀, 암페타민 등 중 독성약물뿐만 아니라 일상 생활에서 흔히 접할 수 있는 흡연, 술 등에 의해서도 그 분비 이상을 초래한다. 따라서 본 논단에서는 최근 뇌신경생물 실험실에서 진행되고 있는 신경전달 물질 중에 도파민 및 GABA 분비에 대 한 연구결과를 바탕으로 소개 하고자 한다.

• Korean Journal of Biological Psychiatry
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• v.17 no.4
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• pp.194-202
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• 2010

Alzheimer's disease(AD) is the most common neurodegenerative disorder and constitutes about two thirds of dementia. Despite a lot of effort to find drugs for AD worldwide, an efficient medicine that can cure AD has not come yet, which is due to the complicated pathogenic pathways and progressively degenerative properties of AD. In its early clinical phase, it is important to find the subtle alterations in synapses responsible for memory because symptoms of AD patients characteristically start with pure impairment of memory. Attempts to find the target synaptic proteins and their pathogenic pathways will be the most powerful alternative strategy for developing AD medicine. Here we review recent progress in deciphering the role of target synaptic proteins related to AD in hippocampal glutamatergic synapses.