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Changes of the Level of G Protein α-subunit mRNA by Withdrawal from Morphine and Butorphanol
Seikwan Oh 대한생리학회-대한약리학회 2000 The Korean Journal of Physiology & Pharmacology Vol.4 No.4
<P> Morphine or butorphanol was continuously infused into cerebroventricle (i.c.v.) with the rate of 26 nmol/ μl/h for 3 days, and the withdrawal from opioid was rendered 7 hrs after the stopping of infusion. The expression of physical dependence produced by these opioids was evaluated by measuring the naloxone- precipitated withdrawal signs. The withdrawal signs produced in animals dependent on butorphanol (<I>kappa</I> opioid receptor agonist) were similar to those of morphine (<I>mu</I> opioid receptor agonist). Besides the behavioral modifications, opioid withdrawal affected G protein expression in the central nervous system. The G-protein α-subunit has been implicated in opioid tolerance and withdrawal. The effects of continuous infusion of morphine or butorphanol on the modulation of G protein α-subunit mRNA were investigated by using in situ hybridization study. In situ hybridization showed that the levels of Gαs and Gαi were changed during opioid withdrawal. Specifically, the level of Gαs mRNA was decreased in the cortex and cerebellar granule layer during the morphine and butorphanol withdrawal. The level of Gαi mRNA was decreased in the dentate gyrus and cerebellar granule layer during the morphine withdrawal. However, the level of Gαi mRNA was significantly elevated during the butorphanol withdrawal. These results suggest that region-specific changes of G protein α-subunit mRNA were involved in the withdrawal from morphine and butorphanol.
오세관(Seikwan Oh) 고려인삼학회 2008 Journal of Ginseng Research Vol.32 No.1
Ginseng saponin has been shown to inhibit the development of dependence on morphine, cocaine, methamphetamine, but the antinarcotics effects of ginseng on nalbuphine remains still largely unknown. Ginseng administration attenuated the naloxone-induced jumping behavior on nalbuphine dependent mice. The development of morphine dependence was mediated through μ-opioid receptor, however, development of nalbuphine dependence was mediated through κ-opioid receptor. However, it was found that the efficacy of analgesic antagonism of GTS was mediated through the serotonergic mechanism, not mediated through the opioid receptor. In addition, ginseng administration modulated cellular signal transduction in the brain. The increased NMDA receptor subunit (NR1, pNR1), phosphate extracellular signal regulated protein kinase (pERK), phosphate cAMP response element binding protein (pCREB) expression by nalbuphine was decreased by the administration of ginseng powder in cortex, hippocampus, striatum of rat brain. These results suggest that ginseng could be one of the targets of antinarcotic therapies to reduce the development of tolerance and dependence on nalbuphine as well as morphine.
Oh, Seikwan,Kim, Hack-Seang,Seong, Yeon-Hee The Pharmaceutical Society of Korea 1995 Archives of Pharmacal Research Vol.18 No.5
These studies were designed to examine the effects of ginsenosides on glutamate neurotansmission. In primary cultures of rat cerebellar granule cells, ginsenosides (Rb1, Rc did not Rg1, $500\mug/ml$) increased glutamate release which was measured by HPLC. but HPLC, but Re did not shwo an elevation of glutamate release. However, all of these ginsenosides down-regulated N-methyl-D-aspartate (NMDA)-induced glutamate release. Rc strongly increased glutamate release and elevated intracellular clcium concentrations $([Ca_{2+}]_i)$ which was measured by ratio fluorometry with FURA-2AM. These results indicate that ginsenosides have a homeostatic effect on glutamate neurotransmission, and there is a structure-function relationship among the ginsenosides tested.
Oh, Seikwan,Moon, Hyung-In,Jung, Jae-Chul,Avery, Mitchell A. Walter de Gruyter GmbH 2008 Zeitschrift für Naturforschung. B, A journal Vol.63 No.11
<B>Abstract</B><P> A simple synthesis, involving a key coupling reaction, and the biological activity of the title compounds 16 and 17 are described. The key fragments are the amine·HCl salt 6 and the acids 9 and 13, which were smoothly coupled by using ethyl(dimethylaminopropyl)carbodiimide (EDCI) and 1- hydroxybenzotriazole (HOBt) in high yield.We have found that the in vitro growth inhibitory potency of the new compounds 16 and 17 exhibits good histone deacetylase (HDAC) activity.</P>
Actoprotective effect of ginseng
Sergiy Oliynyk,Seikwan Oh 고려인삼학회 2013 Journal of Ginseng Research Vol.37 No.2
Actoprotectors are preparations that increase the mental performance and enhance body stability against physical loads without increasing oxygen consumption. Actoprotectors are regarded as a subclass of adaptogens that hold a significant capacity to increase physical performance. The focus of this article is studying adaptogen herbs of genus Panax (P. ginseng in particular) and their capabilities as actoprotectors. Some animal experiments and human studies about actoprotective properties of genus Panax attest that P. ginseng (administered as an extract) significantly increased the physical and intellectual work capacities, and the data provided suggests that ginseng is a natural source of actoprotectors. Preparations of ginseng can be regarded as potential actoprotectors which give way to further research of its influence on physical and mental work capacity, endurance and restoration after exhaustive physical loads while compared with reference actoprotectors.
Yi, Eun-Surk,Oh, Seikwan,Lee, Jang-kyu,Leem, Yea-Hyun Elsevier 2017 Biochemical and biophysical research communication Vol. No.
<P><B>Abstract</B></P> <P>Chronic stress is a precipitating factor for disorders including depression. The basolateral amygdala (BLA) is a critical substrate that interconnects with stress-modulated neural networks to generate emotion- and mood-related behaviors. The current study shows that 3 h per day of restraint stress for 14 days caused mice to exhibit long-term depressive behaviors, manifested by disrupted sociality and despair levels, which were rescued by fluoxetine. These behavioral changes corresponded with morphological and molecular changes in BLA neurons, including chronic stress-elicited increases in arborization, dendritic length, and spine density of BLA principal neurons. At the molecular level, calcium-permeable α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (CP-AMPARs) within the synaptosome exhibited an increased GluR1:GluR2 subunit ratio. We also observed increased GluR1 phosphorylation at Ser 845 and enhanced cyclic AMP-dependent protein kinase (PKA) activity in the BLA. These molecular changes reverted to the basal state post-treatment with fluoxetine. The expression of synaptophysin (SYP) and postsynaptic density protein 95 (PSD-95) at BLA neuronal synapses was also enhanced by chronic stress, which was reversed post-treatment. Finally, chronic stress-provoked depressive behavior was overcome by local blockage of CP-AMPARs in the BLA via stereotaxic injection (IEM-1460). Chronic stress-elicited depressive behavior may be due to hypertrophy of BLA neuronal dendrites and increased of PKA-dependent CP-AMPAR levels in BLA neurons. Furthermore, fluoxetine can reverse chronic stress-triggered cytoarchitectural and functional changes of BLA neurons. These findings provide insights into depression-linked structural and functional changes in BLA neurons.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Chronic stress causes behavioral depression, which is reversed by fluoxetine. </LI> <LI> Chronic stress causes the change of dendritic morphology of BLA neurons. </LI> <LI> Chronic stress increases synaptosomal PKA-dependent CP-AMPARs levels of BLA. </LI> <LI> Chronic stress-induced structural and molecular changes are reversed by fluoxetine. </LI> <LI> Blockage of CP-AMPARs in BLA mitigates stress-elicited depressive phenotype. </LI> </UL> </P>