• Journal of Life Science
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• v.22 no.9
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• pp.1180-1186
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• 2012

The purpose of this study was to investigate the effect of exercise preconditioning (EPC) on nerve growth factor (NGF), synapsin I, and choline acetyltransferase (ChAT) in the hippocampus of rats subjected to social isolation (SI). We randomly assigned four groups of male Sprague-Dawley (SD) rats (n=32) to the following treatments: GC: group housing control; IC: isolation control; GE: group housing exercise; IE: isolation exercise (n=8 each group). The rats underwent EPC 5 days a week for 8 weeks, and the speed of the treadmill was gradually increased (grade $0^{\circ}C$). After EPC, they were immediately subjected to SI for 8 weeks. The results showed that the protein levels of NGF, synapsin I, and ChAT in the hippocampus were significantly decreased in the IC group (p<0.05) compared with the GC group. However, these protein levels were significantly higher in the IE group (p<0.05). These results show that EPC may buffer the decline of function in the hippocampus by ameliorating the reduction in NGF, synapsin I, and ChAT induced by SI.

• The Korean Journal of Physiology and Pharmacology
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• v.4 no.5
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• pp.347-353
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• 2000

It has been well documented that a massive release of not only glutamate but also other neurotransmitters may modulate the final responses of nerve cells to the ischemic neuronal injury. But there is no information regarding whether the release of monoamines is directly associated with synaptic vesicular proteins under ischemia. In the present study, it was investigated whether synapsin 1, syntaxin and SNAP-25 are involved in the release of 5-hydroxytryptamine $([^3H]5-HT)$ in glucose/oxygen deprived (GOD) rat hippocampal slices. And, the effect of NMDA receptor using DL-2-amino-5-phosphonovaleric acid (APV) on ischemia- induced release of 5-HT and the changes of the above proteins were also investigated. GOD for 20 minutes enhanced release of $[^3H]5-HT,$ which was in part blocked by the NMDA receptor antagonist, APV. The augmented expression of synapsin 1 during GOD for 20 minutes, which was also in part prevented by APV. In contrast, the expression of syntaxin and SNAP-25 were not altered during GOD. These results suggest that ischemic insult induces release of $[^3H]5-HT$ associated with synapsin 1, synaptic vesicular protein, via activation of NMDA receptor in part.

• Korean Journal of Biological Psychiatry
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• v.13 no.4
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• pp.260-266
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• 2006

Objectives : Synapsin III near VCFS region on chromosome 22q affects. It could be an interesting candidate gene for schizophrenia. D22S280 is a highly polymorphic genetic marker residing in synapsin III. We examined association of D22S280 marker on synapsin III with Korean patients with schizophrenia. Methods : The subjects were 46 male Korean patients with schizophrenia and 60 male normal controls. Using polymerase chain reaction, gel electrophoresis, ABI 310 genetic analyzer, and GeneScan Collection 3.1 software, we confirmed genotypes of D22S280 marker. We examined Hardy-Weinberg equilibrium and case-control association using SAS/Genetic 9.1.3. Results : Genotypes of both schizophrenia and control groups were in Hardy-Weinberg equilibrium. We could not find any significant statistical differences in allele-wise(${\chi}^2$=10.4, df=6, p=0.098) and genotype-wise (${\chi}^2$=22.1 df=19, p=0.258) analyses of D22S280 marker between schizophrenia and normal controls. Individual allele analyses with df=1 showed significant differences in A1(p=0.025) and A7(p=0.034) allele, which were not significant following Bonferroni corrections(A1:p=0.177, A7:p=0.235). Conclusion : We couldn't find any association between schizophrenia and the synapsin III gene. Given the small number of subjects studied, further investigations are needed.

• The Korean Journal of Physiology and Pharmacology
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• v.8 no.2
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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.

• Molecules and Cells
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• v.38 no.11
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• pp.936-940
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• 2015

Synapsins were the first presynaptic proteins identified and have served as the flagship of the presynaptic protein field. Here we review recent studies demonstrating that different members of the synapsin family play different roles at presynaptic terminals employing different types of synaptic vesicles. The structural underpinnings for these functions are just beginning to be understood and should provide a focus for future efforts.

• 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 Journal of Korean Medicine
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• v.22 no.1
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• pp.78-89
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• 2001

Objectives : The purpose of this investigation is to evaluate the effects of Woohwangcheongsim-won on reperfusion following MCA occlusion in rats. Methods : To evaluate the effect of Woohwangcheongsim-won on reperfusion following MCA occlusion, the volume of cerebral ischemia and edema were measured and the change of the CAI pyramidal neuron in the hippocampus was investigated by light microscopy. And the changes of several neurotransmitters and enzymes were investigated with the immunohistochemical methods. Results : 1. The volume of the control group, which was ischemic-damaged was 23.6%, and that of the sample group was 13.5%. 2. The voluminalratio of the right/left hemisphere was 116 in the control group, and that of the sample group was 107. 3. The pyramidal cells of CAI area in the control group were greatly damaged. The cells were changed into discontinuous and unsystematic forms, and nuclei, and cytoplasms were shrunk. On the other hand, the cells of the sample group were less damaged. 4. On the immunohistochemical methods, the sensitivities of GABA, NOS, DBH in the control group were increased, and those of synapsin and $eEF-l{\alpha}$ were decreased as compared with the normal group. NOS and DBH which were negative in the normal group showed positive reaction. On the other hand, the sensitivities of GABA, NOS and DBH in the sample group were decreased, but those of NPY, synapsin, CaMKII and $eEF-l{\alpha}$ were increased as compared with the control group. Conclusions : Woohwangcheongsim-won reduced the volume of cerebral ischemia and edema, and minimized the damage of pyramidal cells. The mechanism was related to protein synthesis, such as synapsin, ${\alpha}CaMKII$ and $eEF-l{\alpha}$, which resist neurotoxicity of glutamate receptors.

• Applied Microscopy
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• v.48 no.3
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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.

• Biomolecules & Therapeutics
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• v.29 no.6
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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.

• The Journal of Internal Korean Medicine
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• v.22 no.2
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• pp.161-174
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• 2001

Objectives : The purpose of this investigation is to evaluate the effect of Chungpesagan-Tang Extracts on reversible forebrain ischemia in Sprague-Dawley rats. Methods : the volume of cerebral infarction and edema, the pathohistological change of neurons, the number of survived neurons, neurotransmitters through immunohistochemical methods, proteins connected with neurotransmitters through immunohistochemical methods and the pathohistological change of neurons through electro-microscopy were investigated. From these reseach data, the protection of neurons and the activity of brain cells were examined. Results : 1. The infaction volume of the control group was 23.9%, and that of the sample group was 16%. 2. The brain edema volume of the control group increased by 17% compared to the normal group and that of the sample group increased by 10%. 3. The light microscopy revealed that the neurons in the ischemia-induced area and CA1 area of hippocampus were most heavily damaged and that the sample group was less damaged compared with the control group. Most pyramidal neurons died in 7 days when brain ischemia was induced. 4. The number of survived pyramidal neurons in the CA1 area of the hippocampus were studied. The normal group had 93 neurons/mm, survived the control group(after 3 days) had 21/mm, the control group(after 7 days) had 3/mm and the sample group 33/mm. 5. The immunohistochemical methods revealed that: (1) In the control group, the sensitivity of GABA, NOS, DBH were increased, and those of Synapsin, eEF-$1{\alpha}$ decreased. NOS and DBH had positive reactions in the control group, but negative in the normal group. (2) In thd sample group, the sensitivity of GABA, NOS, DBH were attenuated, and those of NPY, Synapsin, CaMKII, eEF-$1{\alpha}$ increased when compared to the control group. 6. The electro-microscopy revealed that most neurons died by necrosis and some neurons died by apoptosis. Several imflammation cells appeared in the injured area of neurons. The number of neurons in the sample group that died by ischemia decreased. But, the number that died by apoptosis did not significantly change. Conclusions : The data shows that the effect of Chungpesagan-Tang Extracts on reversible forebrain ischemia in Sprague-Dawley rats is significant.