• 한국약용작물학회지
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• 제16권1호
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• pp.9-15
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• 2008

Immune-potentiation of Chicorium endivia L. were investigated on follows extracts associated with ultrasonification process at 60 kHz and showed the highest promotion of human B and T cell growth, about $10{\sim}20%$ compared to the control. The secretion of TNF-${\alpha}$ and IL-6 was also enhanced by the addition $(0.5mg/m{\ell})$ of the extracts. NK cell activation was Improved up to 1.37 times higher than the control, through adding extracts. It was also found that extracts from C. endivia L. could yield higher nitric oxide production from macrophage than Lipopolysaccaharides (LPS). It can be concluded that, in general, the extracts treated with ultrasonification has higher immune activity than others, possibly by higher yielding immune-modulatory activity than conventional extraction process. The optimum condition for the extraction of C. endivia L. is ethanol extraction at $60{\sim}100^{\circ}C$ associated with ultrasonification.

• 대한한방내과학회지
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• 제28권2호
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• pp.377-384
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• 2007

Objective : Immune potentiation including activation of T cells, B cells, macrophages, and dendritic cells is known to play a key role in prevention and treatment of patients with cancer. In this study, we investigated the effects of Acanthopanax sessiliflorus (AR) on the immune system, especially on thymocytes, splenocytes, and macrophages. Methods : We investigated the effects of AR on proliferation of splenocytes in normal mice, and the effects on proliferation of splenocytes and thymocytes in tumor-bearing mice. In addition, the effect of AR on NO production using macrophages was investigated. Results : Treatment with AR accelerated proliferation of splenocytes in vitro. AR also accelerated thymocyte proliferation, but did not affect splenocytes proliferation in normal mice. In contrast, AR accelerated proliferation of splenocytes and thymocytes significantly in tumor bearing mice. In addition, NO production level from macrophages was elevated by treatment with AR. Conclusion : These results demonstrate that AR has anti-cancer activities and related mechanisms are involved in immune potentiation such as acceleration of immune cell proliferation and elevation of NO production level in macrophages. In addition, we also demonstrate the possibilities of AR as complementary and alternative medicine to standard anti-cancer drugs.

• Molecules and Cells
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• 제23권3호
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• pp.259-271
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• 2007

Investigation of molecular and cellular mechanisms of synaptic plasticity is the major focus of many neuroscientists. There are two major reasons for searching new genes and molecules contributing to central plasticity: first, it provides basic neural mechanism for learning and memory, a key function of the brain; second, it provides new targets for treating brain-related disease. Long-term potentiation (LTP), mostly intensely studies in the hippocampus and amygdala, is proposed to be a cellular model for learning and memory. Although it remains difficult to understand the roles of LTP in hippocampus-related memory, a role of LTP in fear, a simplified form of memory, has been established. Here, I will review recent cellular studies of LTP in the anterior cingulate cortex (ACC) and then compare studies in vivo and in vitro LTP by genetic/pharmacological approaches. I propose that ACC LTP may serve as a cellular model for studying central sensitization that related to chronic pain, as well as pain-related cognitive emotional disorders. Understanding signaling pathways related to ACC LTP may help us to identify novel drug target for various mental disorders.

• The Korean Journal of Physiology and Pharmacology
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• 제18권6호
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• pp.457-460
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• 2014

At central synapses, activity-dependent synaptic plasticity has a crucial role in information processing, storage, learning, and memory under both physiological and pathological conditions. One widely accepted model of learning mechanism and information processing in the brain is Hebbian Plasticity: long-term potentiation (LTP) and long-term depression (LTD). LTP and LTD are respectively activity-dependent enhancement and reduction in the efficacy of the synapses, which are rapid and synapse-specific processes. A number of recent studies have a strong focal point on the critical importance of another distinct form of synaptic plasticity, non-Hebbian plasticity. Non-Hebbian plasticity dynamically adjusts synaptic strength to maintain stability. This process may be very slow and occur cell-widely. By putting them all together, this mini review defines an important conceptual difference between Hebbian and non-Hebbian plasticity.

• 수면정신생리
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• 제7권1호
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• pp.10-17
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• 2000

To investigate the neurobiological bases of learning and memory is one of the ambitious goals of modern neuroscience. The progress in this field of recent years has not only brought us closer to understanding the molecular mechanism underlying long-lasting changes in synaptic strength, but it has also provided further evidence that these mechanisms are required for memory formation. Since twenty years ago, several studies for the tests of the hypothesis that NMDA-dependent hippocampal long-term potentiation(LTP) underlies learning have been reported. Also, in the recent year, data from mutant mice showed that a potential role for NMDA-dependent LTP in hippocampal CA1 and spatial learning. Although the current evidence for the role of NMDA receptor in learning and memory is not still obvious, NMDA receptor seems to act as a critical switch for activation of a cascade of events that underlie synaptic plasticity.

• 한국환경성돌연변이발암원학회:학술대회논문집
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• 한국환경성돌연변이발암원학회 2003년도 춘계학술대회
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• pp.13-14
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• 2003

• 대한약학회:학술대회논문집
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• 대한약학회 2000년도 NEW STRATEGY FOR DRUG DEVELOPMENT IN POST-GENOMIC ERA(대한약학회)
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• pp.165.2-166
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• 2000

• 대한의용생체공학회:의공학회지
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• 제28권1호
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• pp.17-23
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• 2007

Long-term potentiation (LTP) of synaptic transmission is the most widely studied model for learning and memory. However its mechanisms are not clearly elucidated and are a subject for intense investigation. Previous attempts to decipher cellular mechanisms and network properties involved a current-source density analysis (CSDA) of the LTP from small animal hippocampus measured with a limited number of microelectrodes (typically <3), only revealing limited nature of spatiotemporal dynamics. Recent advancement in multi-electrode array (MEA) technology allows continuous and simultaneous recordings of LTP with more than 60 electrodes. However CSDA via the standard Laplacian transform is still limited due to its relatively high sensitivity toward noise, inability of resolving overlapped current sources and sinks, and its requirement for tissue conductivity values. In this study, we propose a new methodology for improved CSDA. Independent component analysis and its joint use (i.e., Joint-ICA) are applied to extract spatiotemporal components of LTP. The results show that ICA and Joint-ICA are capable of extracting independent spatiotemporal components of LTP generators. The ICs of LTP indicate the reversing roles of current sources and sinks which are associated with LTP.

• The Korean Journal of Physiology and Pharmacology
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• 제17권1호
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• pp.51-56
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• 2013

Many intracellular proteins and signaling cascades contribute to the sensitivity of N-methyl-D-aspartate receptors (NMDARs). One such putative contributor is the serine/threonine kinase, protein kinase C (PKC). Activation of PKC by phorbol 12-myristate 13-acetate (PMA) causes activation of extracellular signal-regulated kinase (ERK) and promotes the formation of new spines in cultured hippocampal neurons. The purpose of this study was to examine which PKC isoforms are responsible for the PMA-induced augmentation of long-term potentiation (LTP) in the CA1 stratum radiatum of the hippocampus in vitro and verify that this facilitation requires NMDAR activation. We found that PMA enhanced the induction of LTP by a single episode of theta-burst stimulation in a concentration-dependent manner without affecting to magnitude of baseline field excitatory postsynaptic potentials. Facilitation of LTP by PMA (200 nM) was blocked by the nonspecific PKC inhibitor, Ro 31-8220 ($10{\mu}M$); the selective $PKC{\delta}$ inhibitor, rottlerin ($1{\mu}M$); and the $PKC{\varepsilon}$ inhibitor, TAT-${\varepsilon}V1$-2 peptide (500 nM). Moreover, the NMDAR blocker DL-APV ($50{\mu}M$) prevented enhancement of LTP by PMA. Our results suggest that PMA contributes to synaptic plasticity in the nervous system via activation of $PKC{\delta}$ and/or $PKC{\varepsilon}$, and confirm that NMDAR activity is required for this effect.

• The Korean Journal of Physiology and Pharmacology
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• 제8권6호
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• pp.295-300
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• 2004

Serotonin (5-hydroxytroptamine, 5-HT) has been shown to affect the induction of long-term potentiation (LTP) in the cortex such as the hippocampus, the visual cortex and the prefrontal cortex. Fluoxetine, as a selective serotonin reuptake inhibitor, is used in the management of a wide variety of psychological diseases. To study the effect of fluoxetine on the induction of LTP, we recorded the field potential in layer II/III of the frontal cortex from 3-wk-old. LTP was induced in horizontal input by theta burst stimulation (TBS). TBS with two-folds intensity of the test stimulation induced LTP, which was blocked by application of D-AP5 $(50 {\mu}M)$, an NMDA receptor antagonist. Whereas bath application of 5-HT $(10 {\mu}M)$ inhibited the induction of LTP, treatment with the 5-HT depleting agent, para-chloroamphetamine $(PCA,\;10{\mu}M)$, for 2hr did not affect the induction of LTP. Bath application of fluoxetine (1, 3, and $10 {\mu}M)$ suppressed the induction of LTP in concentration-dependent manner, however, fluoxetine did not inhibit the induction of LTP in 5-HT-depleted slices. These results indicate that fluoxetine may inhibit the induction of LTP by modulating serotonergic mechanism in the rat frontal cortex.