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The Korean journal of physiology & pharmacology : ... 9건

  1. [국내논문]   Higher Expression of TRPM7 Channels in Murine Mature B Lymphocytes than Immature Cells   피인용횟수: 1

    Kim, Jin-Kyoung (Department of Anesthesiology and Pain Medicine, Samsung Medical Center ) , Ko, Jae-Hong (Department of Physiology and Biophysics, Seoul National University College of Medicine ) , Nam, Joo-Hyun (Department of Physiology, Sungkyunkwan University School of Medicine ) , Woo, Ji-Eun (Department of Physiology, Sungkyunkwan University School of Medicine ) , Min, Kyeong-Min (Department of Physiology, Sungkyunkwan University School of Medicine ) , Earm, Yung-E (Department of Physiology and Biophysics, Seoul National University College of Medicine ) , Kim, Sung-Joon (Department of Physiology and Biophysics, Seoul National University College of Medicine)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.9 no.2 ,pp. 69 - 75 , 2005 , 1226-4512 ,

    초록

    TRPM7, a cation channel protein permeable to various metal ions such as $Mg^{2+}$ , is ubiquitously expressed in variety of cells including lymphocytes. The activity of TRPM7 is tightly regulated by intracellular $Mg^{2+}$ , thus named $Mg^{2+}$ -inhibited cation (MIC) current, and its expression is known to be critical for the viability and proliferation of B lymphocytes. In this study, the level of MIC current was compared between immature (WEHI-231) and mature (Bal-17) B lymphocytes. In both cell types, an intracellular dialysis with $Mg^{2+}$ -free solution (140 mM CsCl) induced an outwardly-rectifying MIC current. The peak amplitude of MIC current and the permeability to divalent cation ( $Mn^{2+}$ ) were several fold higher in Bal-17 than WEHI-231. Also, the level of mRNAs for TRPM7, a molecular correspondence of the MIC channel, was significantly higher in Bal-17 cells. The amplitude of MIC was further increased, and the relation between current and voltage became linear under divalent cation-free conditions, demonstrating typical properties of the TRPM7. The stimulation of B cell receptors (BCR) by ligation with antibodies did not change the amplitude of MIC current. Also, increase of extracellular $[Mg^{2+}]_c$ to enhance the $Mg^{2+}$ influx did not affect the BCR ligation-induced death of WEHI-231 cells. Although the level of TRPM7 was not directly related with the cell death of immature B cells, the remarkable difference of TRPM7 might indicate a fundamental change in the permeability to divalent cations during the development of B cells.

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  2. [국내논문]   Morphine-induced Modulation of Nociceptive Spinal Dorsal Horn Neuronal Activities after Formalin-induced Inflammatory Pain  

    Park, Joo-Min (Department of Physiology, Seoul National University College of Medicine ) , Li, Kang-Wu (Department of Physiology, Seoul National University College of Medicine ) , Jung, Sung-Jin (Department of Physiology, Kangwon National University College of Medicine ) , Kim, Jun (Department of Physiology, Seoul National University College of Medicine ) , Kim, Sang-Jeong (Department of Physiology,Xenotransplantation Research Center, Seoul National University College of Medicine)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.9 no.2 ,pp. 77 - 86 , 2005 , 1226-4512 ,

    초록

    In this study, we examined the morphine-induced modulation of the nociceptive spinal dorsal horn neuronal activities before and after formalin-induced inflammatory pain. Intradermal injection of formalin induced time-dependent changes in the spontaneous activity of nociceptive dorsal horn neurons. In naive cats before the injection of formalin, iontophoretically applied morphine attenuated the naturally and electrically evoked neuronal responses of dorsal horn neurons. However, neuronal responses after the formalin-induced inflammation were significantly increased by morphine. Bicuculline, $GABA_A$ antagonist, increased the naturally and electrically evoked neuronal responses of dorsal horn neurons. This increase in neuronal responses due to bicuculline after the formalin-induced inflammation was larger than that in the naive state, suggesting that basal $GABA_A$ tone increased after the formalin injection. Muscimol, $GABA_A$ agonist, reduced the neuronal responses before the treatment with formalin, but not after formalin treatment, again indicating an increase in the GABAergic basal tone after the formalin injection which saturated the neuronal responses to GABA agonist. Morphine-induced increase in the spinal nociceptive responses after formalin treatment was inhibited by co-application of muscimol. These data suggest that formalin-induced inflammation increases $GABA_A$ basal tone and the inhibition of this augmented $GABA_A$ basal tone by morphine results in a paradoxical morphineinduced increase in the spinal nociceptive neuronal responses after the formalin-induced inflammation.

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  3. [국내논문]   [$Ca^{2+}-induced$ $Ca^{2+}$ Release from Sarcoplasmic Reticulum Negatively Regulates Myocytic ANP Release in Beating Rabbit Atria   피인용횟수: 1

    Li, Dan (Department of Physiology, Institute for Medical Sciences, Institute for Basic Sciences, Jeonbug National University Medical School ) , Quan, He Xiu (Department of Physiology, Institute for Medical Sciences, Institute for Basic Sciences, Jeonbug National University Medical School ) , Wen, Jin-Fu (Department of Physiology, Institute for Medical Sciences, Institute for Basic Sciences, Jeonbug National University Medical School ) , Jin, Jing-Yu (Department of Physiology, Institute for Medical Sciences, Institute for Basic Sciences, Jeonbug National University Medical School ) , Park, Sung-Hun (Department of Physiology, Institute for Medical Sciences, Institute for Basic Sciences, Jeonbug National University Medical School ) , Kim, Sun-Young (Department of Physiology, Institute for Medical Sciences, Institute for Basic Sciences, Jeonbug National University Medical School ) , Kim, Sung-Zoo (Department of Physiology, Institute for Medical Sciences, Institute for Basic Sciences, Jeonbug National University Medical School ) , Cho, Kyung-Woo (Department of Physiology, Institute for Medical Sciences, Institute f)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.9 no.2 ,pp. 87 - 94 , 2005 , 1226-4512 ,

    초록

    It is not clear whether $Ca^{2+}-induced$ $Ca^{2+}$ release from the sarcoplasmic reticulum (SR) is involved in the regulation of atrial natriuretic peptide (ANP) release. Previously, we have shown that nifedipine increased ANP release, indicating that $Ca^{2+}$ entry via voltage-gated L-type $Ca^{2+}$ channel activation decreases ANP release. The purpose of the present study was two-fold: to define the role of SR $Ca^{2+}$ release in the regulation of ANP release and whether $Ca^{2+}$ entry via L-type $Ca^{2+}$ channel is prerequisite for the SR-related effect on ANP release. Experiments were performed in perfused beating rabbit atria. Ryanodine, an inhibitor of SR $Ca^{2+}$ release, increased atrial myocytic ANP release ( $8.69{\pm}3.05$ , $19.55{\pm}1.09$ , $27.31{\pm}3.51$ , and $18.91{\pm}4.76$ % for 1, 2, 3, and $6{\mu}M$ ryanodine, respectively; all P $Ca^{2+}$ pump, ryanodine-induced increase in ANP release was not observed. Thapsigargin attenuated ryanodine-induced decrease in atrial dynamic changes. Blockade of L-type $Ca^{2+}$ channel with nifedipine abolished ryanodine-induced increase in ANP release ( $0.69{\pm}5.58$ % vs. $27.31{\pm}3.51$ %; P<0.001). In the presence of thapsigargin and ryanodine, nifedipine increased ANP release and decreased atrial dynamics. These data suggest that $Ca^{2+}$ -induced $Ca^{2+}$ release from the SR is inversely involved in the regulation of atrial myocytic ANP release.

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  4. [국내논문]   [$Na^+-Ca^{2+}$ Exchange Curtails $Ca^{2+}$before Its Diffusion to Global $Ca^{2+}{_i}$ in the Rat Ventricular Myocyte  

    Ahn, Sung-Wan (Department of Pharmacology and Institute of Basic Medical Science, Yonsei University Wonju-College of Medicine ) , Ko, Chang-Mann (Department of Pharmacology and Institute of Basic Medical Science, Yonsei University Wonju-College of Medicine)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.9 no.2 ,pp. 95 - 101 , 2005 , 1226-4512 ,

    초록

    In the heart, $Na^{+}-Ca^{2+}$ exchange (NCX) is the major $Ca^{2+}$ extrusion mechanism. NCX has been considered as a relaxation mechanism, as it reduces global $[Ca^{2+}]_i$ raised during activation. However, if NCX locates in the close proximity to the ryanodine receptor, then NCX would curtail $Ca^{2+}$ before its diffusion to global $Ca^{2+}_i$ This will result in a global $[Ca^{2+}]_i$ decrease especially during its ascending phase rather than descending phase. Therefore, NCX would decrease the myocardial contractility rather than inducing relaxation in the heart. This possibility was examined in this study by comparing NCX-induced extrusion of $Ca^{2+}$ after its release from SR in the presence and absence of global $Ca^{2+}_i$ transient in the isolated single rat ventricular myocytes by using patch-clamp technique in a whole-cell configuration. Global $Ca^{2+}_i$ transient was controlled by an internal dialysis with different concentrations of BAPTA added in the pipette. During stimulation with a ramp pulse from +100 mV to -100 mV for 200 ms, global $Ca^{2+}_i$ transient was suppressed only mildly, and completely at 1 mmol/L, and 10 mmol/L BAPTA, respectively. In these situations, ryanodine-sensitive inward NCX current was compared using $100{\mu}mol/L$ ryanodine, $Na^+$ depletion, 5 mmol/L $NaCl_2$ and $1{\mu}mol/L$ nifedipine. Surprisingly, the result showed that the ryanodine-sensitive inward NCX current was well preserved after 10 mmol/L BAPTA to 91 % of that obtained after 1 mmol/L BAPTA. From this result, it is concluded that most of the NCX-induced $Ca^{2+}$ extrusion occurs before the $Ca^{2+}$ diffuses to global $Ca^{2+})i$ in the rat ventricular myocyte.

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  5. [국내논문]   Regulation of L-type Calcium Channel Current by Somatostatin in Guinea-Pig Gastric Myocytes  

    Kim, Young-Chul (Department of Physiology, Chungbuk National University College of Medicine ) , Sim, Jae-Hoon (Department of Physiology and Biophysics, Seoul National University College of Medicine ) , Lee, Sang-Jin (Department of Physiology, Chungbuk National University College of Medicine ) , Kang, Tong-Mook (Department of Physiology, Sungkyunkwan University School of Medicine ) , Kim, Sung-Joon (Department of Physiology and Biophysics, Seoul National University College of Medicine ) , Kim, Seung-Ryul (Department of Biochemistry, Chungbuk National University College of Medicine ) , Youn, Sei-Jin (Department of Internal Medicine, Chungbuk National University College of Medicine ) , Lee, Sang-Jeon (Department of Surgery, Chungbuk National University College of Medicine ) , Xu, Wen Xie (Department of Physiology, Medical School, Shaghai Jiao Tong University ) , So, In-Suk (Department of Physiology and Biophysics, Seoul National University College of Medicine ) , Kim, Ki-Whan (Department of Physiology and Biophysics, Seoul National University College of Medicine)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.9 no.2 ,pp. 103 - 108 , 2005 , 1226-4512 ,

    초록

    To study the direct effect of somatostatin (SS) on calcium channel current ( $I_{Ba}$ ) in guinea-pig gastric myocytes, $I_{Ba}$ was recorded by using whole-cell patch clamp technique in single smooth muscle cells. Nicardipine ( $1{\mu}M$ ), a L-type $Ca^{2+}$ channel blocker, inhibited $I_{Ba}$ by $98{\pm}1.9$ % (n=5), however $I_{Ba}$ was decreased in a reversible manner by application of SS. The peak $I_{Ba}$ at 0 mV were decreased to $95{\pm}1.5$ , $92{\pm}1.9$ , $82{\pm}4.0$ , $66{\pm}5.8$ , $10{\pm}2.9$ % at $10^{-10}$ , $10^{-9}$ , $10^{-8}$ , $10^{-7}$ , $10^{-5}$ M of SS, respectively (n=3∼6; $mean{\pm}SEM$ ). The steady-state activation and inactivation curves of $I_{Ba}$ as a function of membrane potentials were well fitted by a Boltzmann equation. Voltage of half-activation ( $V_{0.5}$ ) was $-12{\pm}0.5$ mV in control and $-11{\pm}1.9$ mV in SS treated groups (respectively, n=5). The same values of half-inactivation were $-35{\pm}1.4$ mV and $-35{\pm}1.9$ mV (respectively, n=5). There was no significant difference in activation and inactivation kinetics of $I_{Ba}$ by SS. Inhibitory effect of SS on $I_{Ba}$ was significantly reduced by either dialysis of intracellular solution with $GDP_{\beta}S$ , a non-hydrolysable G protein inhibitor, or pretreatment with pertussis toxin (PTX). SS also decreased contraction of guinea-pig gastric antral smooth muscle. In conclusion, SS decreases voltage-dependent L-type calcium channel current ( $VDCC_L$ ) via PTXsensitive signaling pathways in guinea-pig antral circular myocytes.

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  6. [국내논문]   Enhanced Expression of Cell Adhesion Molecules in the Aorta of Diabetic Mice is Mediated by gp91phox-derived Superoxide  

    Yun, Mi-Ran (Department of Pharmacology, College of Medicine, Research Institute of Genetic Engineering, Pusan National University ) , Kim, Jong-Jae (Department of Pharmacology, College of Medicine, Research Institute of Genetic Engineering, Pusan National University ) , Lee, Sun-Mi (Department of Pharmacology, College of Medicine, Research Institute of Genetic Engineering, Pusan National University ) , Heo, Hye-Jin (Department of Pharmacology, College of Medicine, Research Institute of Genetic Engineering, Pusan National University ) , Bae, Sun-Sik (Department of Pharmacology, College of Medicine, Research Institute of Genetic Engineering, Pusan National University ) , Kim, Chi-Dae (Department of Pharmacology, College of Medicine, Research Institute of Genetic Engineering, Pusan National University)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.9 no.2 ,pp. 109 - 115 , 2005 , 1226-4512 ,

    초록

    Endothelial activation and subsequent recruitment of inflammatory cells are important steps in atherogenesis. The increased levels of cell adhesion molecules (CAM) have been identified in diabetic vasculatures, but the underlying mechanisms remain unclear. To determine the relationship among vascular production of superoxide, expression of CAM and diabetes, superoxide generation and expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), E- and P-selectin in the aorta from control (C57BL/6J) and diabetic mice (ob/ob) were measured. In situ staining for superoxide using dihydroethidium showed an increased superoxide production in diabetic aorta, accompanied with an enhanced NAD(P)H oxidase activity. Immunohistochemical analysis revealed that the endothelial expression of ICAM-1 ( $3.5{\pm}0.4$ ) and VCAM-1 ( $3.8{\pm}0.3$ ) in diabetic aorta was significantly higher than those in control aorta ( $0.9{\pm}0.5$ and $1.6{\pm}0.3$ , respectively), accompanied with the enhanced expression of gp91phox, a membrane subunit of NAD(P)H oixdase. Furthermore, there was a strong positive correlation (r=0.89, P<0.01 in ICAM-1 and r=0.88, P<0.01 in VCAM-1) between ICAM-1/VCAM-1 expression and vascular production of superoxide. The present data indicate that the increased production of superoxide via NAD(P)H oxidase may explain the enhanced expression of CAM in diabetic vasculatures.

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  7. [국내논문]   Inhibition of Angiotensin II-Induced Vascular Smooth Muscle Cell Hypertrophy by Different Catechins   피인용횟수: 2

    Zheng, Ying (Department of Pharmacology, College of Medicine, Chungbuk National University ) , Song, Hye-Jin (Department of Pharmacology, College of Medicine, Chungbuk National University ) , Yun, Seok-Hee (Department of Pharmacology, College of Medicine, Chungbuk National University ) , Chae, Yeon-Jeong (Department of Pharmacology, College of Medicine, Chungbuk National University ) , Jia, Hao (Department of Pharmacology, College of Medicine, Chungbuk National University ) , Kim, Chan-Hyung (Department of Pharmacology, College of Medicine, Chungbuk National University ) , Ha, Tae-Sun (Department of Pediatrics, College of Medicine, Chungbuk National University ) , Sachinidis, Agapios (Center of Physiology and Pathophysiology, University of Cologne ) , Ahn, Hee-Yul (Department of Pharmacology, College of Medicine, Chungbuk National University ) , Davidge, Sandra T. (Department of Obstetrics and Gynecology and Physiology, Perinatal Research Center, University of Alberta)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.9 no.2 ,pp. 117 - 123 , 2005 , 1226-4512 ,

    초록

    A cumulative evidence indicates that consumption of tea catechin, flavan-3-ol derived from green tea leaves, lowers the risk of cardiovascular diseases. However, a precise mechanism for this cardiovascular action has not yet been fully understood. In the present study, we investigated the effects of different green tea catechins, such as epigallocatechin-3 gallate (EGCG), epigallocatechin (EGC), epicatechin-3 gallate (ECG), and epicatechin (EC), on angiotensin II (Ang II)-induced hypertrophy in primary cultured rat aortic vascular smooth muscle cell (VSMC). [ $^3H$ ]-leucine incorporation was used to assess VSMC hypertrophy, protein kinase assay, and western blot analysis were used to assess mitogen-activated protein kinase (MAPK) activity, and RT-PCR was used to assess c-jun or c-fos transcription. Ang II increased [ $^3H$ ]-leucine incorporation into VSMC. However, EGCG and ECG, but not EGC or EC, inhibited [ $^3H$ ]-leucine incorporation increased by Ang II. Ang II increased phosphorylation of c-Jun, extracellular-signal regulated kinase (ERK) 1/2 and p38 MAPK in VSMC, however, EGCG and ECG , but not EGC or EC, attenuated c-Jun phosphorylation increased by Ang II. ERK 1/2 and p38 MAPK phosphorylation induced by Ang II were not affected by any catechins. Ang II increased c-jun and c-fos mRNA expression in VSMC, however, EGCG inhibited c-jun but not c-fos mRNA expression induced by Ang II. ECG, EGC and EC did not affect c-jun or c-fos mRNA expression induced by Ang II. Our findings indicate that the galloyl group in the position 3 of the catechin structure of EGCG or ECG is essential for inhibiting VSMC hypertrophy induced by Ang II via the specific inhibition of JNK signaling pathway, which may explain the beneficial effects of green tea catechin on the pathogenesis of cardiovascular diseases observed in several epidemiological studies.

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  8. [국내논문]   Insulin Resistance of Skeletal Muscle was Recovered by Leptin Injection in vivo, but not in vitro, in High-fat Diet Fed Rats  

    Doh, Kyung-Oh (Department of Physiology, Yeungnam University College of Medicine ) , Park, Jeong-Oak (Department of Physiology, Yeungnam University College of Medicine ) , Jeon, Jeong-Ryne (Department of Physiology, Yeungnam University College of Medicine ) , Kim, Jong-Yeon (Department of Physiology, Yeungnam University College of Medicine)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.9 no.2 ,pp. 125 - 130 , 2005 , 1226-4512 ,

    초록

    We examined the effect of leptin on the insulin resistance in skeletal muscles by measuring the glucose transport. Male Wistar rats were fed with chow or high-fat diets for 30 days. Three days before sacrifice, high-fat fed rats were subcutaneously injected with leptin (1 mg/kg body weight) for 3 days. The glucose transports in the epitrochlearis and soleus muscle were not different among the experimental groups under basal state, however these were decreased significantly in the high fat-diet rats under insulin-stimulation (p<0.01). Leptin treatment recovered the decreased glucose transport in the epitrochlearis (p<0.05) and soleus (p=0.08). Triglyceride concentration in the soleus muscle was increased significantly in the high fat-fed rats, compared to chow diet rats (p<0.01), and it was decreased significantly by leptin treatment (p<0.01). The glucose transport was measured under basal and $60{\mu}u/ml$ of insulin with or without 50 ng/ml of leptin. Leptin had no direct stimulatory effect on glucose transport under both basal and insulin-stimulated conditions in vitro. These results demonstrate that leptin injection to high fat diet fed rats recovered impaired insulin responsiveness of the skeletal muscles and muscle triglyceride concentration. However, there was no direct stimulatory effect of leptin on insulin sensitivity of the skeletal muscle in vitro.

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  9. [국내논문]   Modulation of Large Conductance $Ca^{2+}-activated$ $K^+4$ Channel of Skin Fibroblast (CRL-1474) by Cyclic Nucleotides  

    Yun, Ji-Hyun (Department of Physiology, College of Medicine, Chung-Ang University ) , Kim, Seung-Tae (Department of Physiology, College of Medicine, Chung-Ang University ) , Bang, Hyo-Weon (Department of Physiology, College of Medicine, Chung-Ang University)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.9 no.2 ,pp. 131 - 135 , 2005 , 1226-4512 ,

    초록

    Potassium channels in human skin fibroblast have been studied as a possible site of Alzheimer disease pathogenesis. Fibroblasts in Alzheimer disease show alterations in signal transduction pathway such as changes in $Ca^{2+}$ homeostasis and/or $Ca^{2+}-activated$ kinases, phosphatidylinositol cascade, protein kinase C activity, cAMP levels and absence of specific $K^+$ channel. However, little is known so far about electrophysiological and pharmacological characteristics of large-conductance $Ca^{2+}$ -activated $K^+$ ( $BK_{Ca}$ ) channel in human fibroblast (CRL-1474). In the present study, we found Iberiotoxin- and TEA-sensitive outward rectifying oscillatory current with whole-cell recordings. Single channel analysis showed large conductance $K^{+}$ channels (106 pS of chord conductance at +40 mV in physiological $K^+$ gradient). The 106 pS channels were activated by membrane potential and $[Ca^{2+}]_i$ , consistent with the known properties of $BK_{Ca}$ channels. $BK_{Ca}$ channels in CRL-1474 were positively regulated by adenylate cyclase activator ( $10{\mu}M$ forskolin), 8-Br-cyclic AMP ( $300{\mu}M$ ) or 8-Br-cyclic GMP ( $300{\mu}M$ ). These results suggest that human skin fibroblasts (CR-1474) have typical $BK_{Ca}$ channel and this channel could be modulated by c-AMP and c-GMP. The electrophysiological characteristics of fibroblasts might be used as the diagnostic clues for Alzheimer disease.

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