• 생명과학회지
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• 제22권9호
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• pp.1180-1186
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• 2012

본 연구는 사회적 고립 스트레스로 인한 해마에서의 nerve growth factor (NGF), Synapsin I 및 choline acetyltranferase (ChAT) 감소에 있어서 사전운동경험(exercise preconditioning: EPC)이 미치는 영향을 규명하고자 실시되었다. 목적을 위해 Sprague-Dawley (SD) 쥐(수컷, 22주령, $500.1{\pm}48.41$ g)를 이용해 크게 통제집단(Con)과 운동(Ex)집단으로 구분하여 운동(트레드밀, 5일/주, 최대 18-20 m/min; 50분까지 점진적 증가, 경사 없음, 8주)을 적용하였으며, 이후 각각 사회적 고립(Isolation, 8주)을 적용하여 분석하였다(Group/Con: GC, Group/Ex: GE, Isolation/Con: IC, Isolation/Ex: IE, 각 집단별 n=8). 실험결과, IC집단에서 GC집단에 비해 해마에서 NGF, Synapsin I 및 ChAT가 유의하게 감소한 것으로 나타났다. 반면 IE집단에서 IC집단에 비해 NGF, Synapsin I 및 ChAT의 감소가 유의하게 개선된 것으로 나타났다. 이상의 결과 사회적 고립에 의한 해마에서의 NGF, Synapsin I 및 ChAT 단백질 감소는 EPC에 의해 개선되며, 이를 통해 해마의 기능 저하를 일부 완충 시킬 수 있을 것으로 판단된다.

• The Korean Journal of Physiology and Pharmacology
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• 제8권2호
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• pp.77-81
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• 2004

The loss of neurons and synaptic contacts following cerebral ischemia may lead to a synaptic plastic modification, which may contribute to the functional recovery after a brain lesion. Using synapsin I and GAP-43 as markers, we investigated the neuronal cell death and the synaptic plastic modification in the rat hippocampus of a middle cerebral artery occlusion (MCAO) model. Cresyl violet staining revealed that neuronal cell damage occurred after 2 h of MCAO, which progressed during reperfusion for 2 weeks. The immunoreactivity of synapsin I and GAP-43 was increased in the stratum lucidum in the CA3 subfield as well as in the inner and outer molecular layers of dentate gyrus in the hippocampus at reperfusion for 2 weeks. The immunoreactivity of phosphosynapsin was increased in the stratum lucidum in the CA3 subfield during reperfusion for 1 week. Our data suggest that the increase in the synapsin I and GAP-43 immunoreactivity probably mediates either the functional adaptation of the neurons through reactive synaptogenesis from the pre-existing presynaptic nerve terminals or the structural remodeling of their axonal connections in the areas with ischemic loss of target cells. Furthermore, phosphosynapsin may play some role in the synaptic plastic adaptations before or during reactive synaptogenesis after the MCAO.

• PNF and Movement
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• 제6권2호
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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.

• Biomolecules & Therapeutics
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• 제29권6호
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• pp.630-636
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• 2021

Eupafolin, a constituent of the aerial parts of Phyla nodiflora, has neuroprotective property. Because reducing the synaptic release of glutamate is crucial to achieving pharmacotherapeutic effects of neuroprotectants, we investigated the effect of eupafolin on glutamate release in rat cerebrocortical synaptosomes and explored the possible mechanism. We discovered that eupafolin depressed 4-aminopyridine (4-AP)-induced glutamate release, and this phenomenon was prevented in the absence of extracellular calcium. Eupafolin inhibition of glutamate release from synaptic vesicles was confirmed through measurement of the release of the fluorescent dye FM 1-43. Eupafolin decreased 4-AP-induced [Ca²⁺]_i elevation and had no effect on synaptosomal membrane potential. The inhibition of P/Q-type Ca²⁺ channels reduced the decrease in glutamate release that was caused by eupafolin, and docking data revealed that eupafolin interacted with P/Q-type Ca²⁺ channels. Additionally, the inhibition of calcium/calmodulin-dependent protein kinase II (CaMKII) prevented the effect of eupafolin on evoked glutamate release. Eupafolin also reduced the 4-AP-induced activation of CaMK II and the subsequent phosphorylation of synapsin I, which is the main presynaptic target of CaMKII. Therefore, eupafolin suppresses P/Q-type Ca²⁺ channels and thereby inhibits CaMKII/synapsin I pathways and the release of glutamate from rat cerebrocortical synaptosomes.

• Applied Microscopy
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• 제48권3호
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• pp.55-61
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• 2018

The synaptic vesicle is a specialized structure in presynaptic terminals that stores various neurotransmitters. The actin filament has been proposed for playing an important role in mobilizing synaptic vesicles. To understand the role of actin filament on synaptic vesicle pooling, we characterized synaptic vesicles and actin filament after treatment of brain-derived neurotrophic factor (BDNF) or Latrunculin A on primary cultured neuron from rat embryo hippocampus. Western blots revealed that BDNF treatment increased the expression of synapsin I protein, but Latrunculin A treatment decreased the synapsin I protein expression. The increased expression of synapsin I after BDNF disappeared by the treatment of Latrunculin A. Three-dimensional (3D) tomography of synapse showed that more synaptic vesicles localized near the active zone and total number of synaptic vesicles increased after treatment of BDNF. But the number of synaptic vesicle was 2.5-fold reduced in presynaptic terminals and the loss of filamentous network was observed after Latrunculin A application. The treatment of Latruculin A after preincubation of BDNF group showed that synaptic vesicle number was similar to that of control group, but filamentous structures were not restored. These data suggest that the actin filament plays a significant role in synaptic vesicles pooling in presynaptic terminals.