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The Korean journal of physiology & pharmacology : ... 16건

  1. [국내논문]   Differential Inhibitory Action of Taurine between Electrically Evoked Response and Low $Mg^{++}-Induced$ Spontaneous Activity in the CA1 Area of the Rat Hippocampal Slices  

    Baek, Soo-Youn (Department of Biology, College of Natural Science, Inha University ) , Yang, Sung-Gu (Department of Biology, College of Natural Science, Inha University ) , Lee, Chang-Joong (Department of Biology, College of Natural Science, Inha University)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.5 ,pp. 467 - 475 , 1997 , 1226-4512 ,

    초록

    Although one of the major physiological functions of taurine(2-aminoethanesulfonic acid) is the inhibitory action on the central nervous system(CNS), the mechanism of taurine in controlling the neuronal excitation in the CNS has been in controversy. Electrically evoked pEPSP and spontaneous activity induced by the perfusion of low $Mg^{++}-ACSF$ were recorded in the CA1 pyramidal cell layer of the hippocampal slice. To test the inhibitory effect of taurine on spontaneous responses, taurine was treated for 2 min at various concentrations(1 mM-10 mM). Taurine reduced the spontaneous activity by 22.2% at 1 mM, and 100% at 2 mM in low $Mg^{++}-ACSF$ . Evoked response was induced by electrical stimulation of Schaffer collateral-commissural fibers. Taurine reduced the evoked response by 11.68% at 3 mM, and 24.25% at 5 mM. Even 20 mM of taurine reduced the evoked response only by 24 % after 5 min treatment. That is, the inhibitory efficacy was much higher in spontaneous activity than in evoked response. The $GABA_A$ receptor antagonist, 100 uM bicuculline, blocked the inhibitory action of taurine, while $GABA_B$ receptor antagonist, 700 uM phaclofen, did not. Taurine blocked the spontaneous activity in the presence of CNQX, and did not block the electrically evoked responce in the presence of APV. The results suggest that taurine causes hyperpolarization in the cell by binding to $GABA_A$ receptor and preferentially attenuates NMDA receptor-mediated hyperexcitation, leaving synaptic transmission unmodified.

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  2. [국내논문]   Blockade of Intrinsic Oscillatory Activity of Cerebellar Purkinje Cells by Apamin and Nickel  

    Seo, Wha-Sook (Department of Nursing, College of Medicine Inha University ) , Strahlendorf, Jean-C. (Departments of Physiology, Texas Tech University Health Sciences Center ) , Strahlendorf, Howard-K. (Departments of Pharmacology, Texas Tech University Health Sciences Center)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.5 ,pp. 477 - 484 , 1997 , 1226-4512 ,

    초록

    Intracellular recordings of oscillatory firing (bursting activity) were obtained from Purkinje cells (PCs) in rat cerebellar slices. Apamin inhibited post-burst hyperpolarizations (PBHs) progressively and finally terminated oscillatory firing activity of PCs. Apamin did not affect the amplitude or duration of the after-hyperpolarization (AHP) between spikes within the burst. In the voltage clamp mode, apamin shifted the whole-cell, quasi-steady state I/V relationship in an inward direction and abolished the zero slope resistance (ZSR) region by blocking outward current. Nickel ( $Ni^{2+}$ ) terminated oscillatory activity and also abolished the ZSR region. However, $Ni^{2+}$ did not have progressive blocking action on the post-burst hyperpolarization before it blocked oscillatory activity. $Ni^{2+}$ blocked an inward current at potentials positive to approximately -65 mV, which was responsible for the ZSR region and outward current at more negative potentials. These data indicated that oscillatory activity of PCs is sustained by a balance between a slow $Ni^{2+}$ -sensitive inward current and an apamin-sensitive outward current in the region of ZSR of the whole-cell I/V curve.

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  3. [국내논문]   [${\alpha}-Adrenergic$ and Cholinergic Receptor Agonists Modulate Voltage-Gated $Ca^{2+}$ Channels  

    Nah, Seung-Yeol (Department of Physiology, College of Veterinary Medicine, Chonnam National University ) , Kim, Jae-Ha (Department of Pharmacology, College of Medicine, Chonnam National University ) , Kim, Cheon-Ho (Department of Veterinary Medicine, Kangwon National University)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.5 ,pp. 485 - 493 , 1997 , 1226-4512 ,

    초록

    We investigated the effect of ${\alpha}-adrenergic$ and cholinergic receptor agonists on $Ca^{2+}$ current in adult rat trigeminal ganglion neurons using whole-cell patch clamp methods. The application of acetylcholine, carbachol, and oxotremorine ( $50\;{\mu}M\;each$ ) produced a rapid and reversible reduction of the $Ca^{2+}$ current by $17{\pm}6%,\;19{\pm}3%,\;and\;18{\pm}4%$ , respectively. Atropine, a muscarinic antagonist, blocked carbachol- induced $Ca^{2+}$ current inhibition to $3{\pm}1%$ . Norepinephrine ( $50\;{\mu}M$ ) reduced $Ca^{2+}$ current by $18{\pm}2%$ , while clonidine ( $50\;{\mu}M$ ), an ${\alpha}2-adrenergic$ receptor agonist, inhibited $Ca^{2+}$ current by only $4{\pm}1%$ . Yohimbine, an ${\alpha}2-adrenergic$ receptor antagonist, did not block the inhibitory effect of norepinephrine on $Ca^{2+}$ current, whereas prazosin, an ${\alpha}1-adrenergic$ receptor antagonist, attenuated the inhibitory effect of norepinephrine on $Ca^{2+}$ current to $6{\pm}1%$ . This pharmacology contrasts with ${\alpha}2-adrenergic$ receptor modulation of $Ca^{2+}$ channels in rat sympathetic neurons, which is sensitive to clonidine and blocked by yohimbine. Our data suggest that the modulation of voltage dependent $Ca^{2+}$ channel by norepinephrine is mediated via an α1-adrenergic receptor. Pretreatment with pertussis toxin (250 ng/ml) for 16 h greatly reduced norepinephrine- and carbachol-induced $Ca^{2+}$ current inhibition from $17{\pm}3%\;and\;18{\pm}3%\;to\;2{\pm}1%\;and\;2{\pm}1%$ , respectively. These results demonstrate that norepinephrine, through an ${\alpha}1-adrenergic$ receptor, and carbachol, through a muscarinic receptor, inhibit $Ca^{2+}$ currents in adult rat trigeminal ganglion neurons via pertussis toxin sensitive GTP-binding proteins.

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  4. [국내논문]   Regulation of AQP-4 Water Channel Expression in the Brain during Development and by Ischemia  

    Jung, Jin-Sup (Department of Physiology, College of Medicine, Pusan National University ) , Kim, Hae-Gyu (Department of Anesthesiology, College of Medicine, Pusan National University ) , Bae, Hae-Rahn (Department of Physiology, College of Medicine and Dong-A University ) , Suh, Duk-Joon (Department of Physiology, College of Medicine and Dong-A University ) , Park, Hwan-Tae (Department of Anatomy, College of Medicine, Inje University ) , Lee, Sang-Ho (Department of Physiology College of Medicine, Pusan National University)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.5 ,pp. 495 - 504 , 1997 , 1226-4512 ,

    초록

    Water transport is mediated by two distinct pathways, diffusional and channel-mediated water transport. The first molecular water channel was identified from human erythrocytes in 1992. Genetically-related proteins from other mammalian tissues have subsequently been identified to transport water, and the group is referred to as th "Aquaporins". Aquaporin-4 (AQP4) is most abundant in the brain, which may be involved in CSF reabsorption and osmoregulation. However, ontogeny and regulatory mechanisms of AQP4 channels have not been reported. Northern blot analysis showed that AQP4 mRNA began to be expressed in the brain just before birth and that its expression gradually increased by PN7 and then decreased at adult level. AQP4 was expressed predominantly in the ependymal cells of ventricles in newborn rats. And then its expression decreased in ependymal cells and increased gradually in other regions including supraoptic and paraventricular nuclei. AQP4 is also expressed in the subfornical organ, in which the expression level is not changed after birth. Cryogenic brain injury did not affect expression of AQP4 mRNA, while ischemic brain injury decreased it. Osmotic water permeability of AQP4 channel expressed in Xenopus oocytes was inhibited by the pretreatment of BAPTA/AM and calmidazolium, a $Ca^{2+}/Calmodulin$ kinase inhibitor, in a dose-dependent manner. These results indicate that the expression and the function of AQP4 channel are regulated by developmental processes and various pathophysiological conditions. These results will contribute to the understanding of fluid balance in the central nervous system and the osmoregulatory mechanisms of the body.

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  5. [국내논문]   Correlation Between Electrical Activity of Type I Neuron and c-Fos Expression in the Medial Vestibular Nuclei Following Unilateral Labyrinthectomy in Rats  

    Park, Byung-Rim (Department of Physiology, Wonkwang University School of Medicine, and Medicinal Resources Research Center of Wonkwang University ) , Doh, Nam-Yong (Department of Otolaryngology, Chosun University Medical College ) , Kim, Min-Sun (Department of Physiology, Wonkwang University School of Medicine, and Medicinal Resources Research Center of Wonkwang University ) , Chun, Sang-Woo (Department of Physiology, Wonkwang University School of Medicine, and Medicinal Resources Research Center of Wonkwang University ) , Lee, Moon-Young (Department of Physiology, Wonkwang University School of Medicine, and Medicinal Resources Research Center of Wonkwang University ) , Lee, Sung-Ho (Department of Physiology, Wonkwang University School of Medicine, and Medicinal Resources Research Center of Wonkwang University)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.5 ,pp. 505 - 513 , 1997 , 1226-4512 ,

    초록

    To search the correlations between electrical activity and c-Fos expression in the process of vestibular compensation, we examined the changes of those two parameters in the medial vestibular nuclei (MVN) of unilaterally labyrinthectomized (ULX) rats. Spontaneous nystagmus with fast component toward the intact side disappeared gradually within 48 hours. Fourty eight hours after ULX, directional preponderance of the eye movement induced by sinusoidal rotation of the whole body which represents the symmetry of bilateral vestibular functions showed less than 20% by rotation of 0.1, 0.2, and 0.5 Hz, indicating the recovery of symmetry in bilateral vestibular functions. Six hours after ULX, spontaneous electrical activity of type I neurons resulted in asymmetry between bilateral MVN, however, the asymmetry of the electrical activity was decreased 48 hours after ULX. Immunocytochemical staining revealed that ULX produced dramatic induction of c-Fos positive cells in the MVN bilaterally. The number of c-Fos immunoreactive cells in the contralateral MVN was significantly higher than those in the ipsilateral MVN (p<0.0001) 2 hours after ULX. Thereafter, the number of c-Fos positive cells decreased bilaterally and was slightly, but not significantly higher in the ipsilateral MVN at 48 hours after ULX. The present results suggest that both electrical activity of type I neurons and c-Fos expression in MVN following ULX will reflect underlying mechanisms of recovery process of vestibular compensation.

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  6. [국내논문]   Nitric Oxide Prevents the Bovine Cerebral Endothelial Cell Death Induced by Serum-Deprivation  

    Kim, Chul-Hoon (Yonsei Brain Research Institute and Department of Pharmacology, Yonsei University College of Medicine ) , Ahn, Young-Soo (Yonsei Brain Research Institute and Department of Pharmacology, Yonsei University College of Medicine)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.5 ,pp. 515 - 521 , 1997 , 1226-4512 ,

    초록

    Endothelial cells play a central role in the inflammatory processes, and activation of nuclear factor kappa B ( $NF-_{\kappa}B$ ) is a key component in that inflammatory processes. Previously, we reported that tumor necrosis factor alpha( $TNF{\alpha}$ ) had protective effect of cell death induced by serum deprivation and this protection was related to $NF-_{\kappa}B$ activation. Inducible nitric oxide synthase (iNOS) is a member of the molecules which transcription is regulated mainly by $NF-_{\kappa}B$ . And the role of nitric oxide (NO) generated by iNOS on cell viability is still controversial. To elucidate the mechanism of $TNF{\alpha}$ and $NF-_{\kappa}B$ activation on cell death protection, we investigate the effect of NO on the cell death induced by serum- deprivation in bovine cerebral endothelial cells in this study. Addition of $TNF{\alpha}$ , which are inducer of iNOS, prevented serum-deprivation induced cell death. Increased expression of iNOS was confirmed indirectly by nitrite measurement. When selective iNOS inhibitors were treated, the protective effect of $TNF{\alpha}$ on cell death was partially blocked, suggesting that iNOS expression was involved in controlling cell death. Exogenously added NO substrate (L-arginine) and NO donors (sodium nitroprusside and S-nitroso-N-acetylpenicillamine) also inhibited the cell death induced by serum deprivation. These results suggest that NO has protective effect on bovine cerebral endothelial cell death induced by serum-deprivation and that iNOS is one of the possible target molecules by which $NF-_{\kappa}B$ exerts its cytoprotective effect.

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  7. [국내논문]   Changes of Renal Peripheral Benzodiazepine Receptor in the Stress/Anxiety Response  

    Ha, Jeoung-Hee (Department of Pharmacology, College of Medicine, Yeungnam University ) , Lee, Kwang-Hun (Department of Psychiatry, College of Medicine, Dongook University ) , Cheung, Seung-Douk (Department of Psychiatry, College of Medicine, Yeungnam University ) , Park, Hyung-Bae (Department of Psychiatry, College of Medicine, Yeungnam University ) , Lee, Maan-Gee (Department of Pharmacology, College of Medicine, Kyungpook National University ) , Choi, Hyoung-Chul (Department of Pharmacology, College of Medicine, Yeungnam University ) , Sohn, Uy-Dong (Department of Pharmacology, College of Medicine, Yeungnam University ) , Lee, Kwang-Youn (Department of Pharmacology, College of Medicine, Yeungnam University ) , Kim, Won-Joon (Department of Pharmacology, College of Medicine, Yeungnam University)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.5 ,pp. 523 - 528 , 1997 , 1226-4512 ,

    초록

    Peripheral benzodiazepine receptor(PBR) has been indentified in various peripheral tissues including kidney. The physiological and pharmacological functions of PBR are still uncertain, althought it has been suggested that these are associated with the regulation of stress/anxiety response. Diazepam progeny, which were exposed to diazepam perinatally, was reported to be an animal model of chronic anxiety. However, PBR in the diazepam progenies are not known yet. In the present study, therefore, we examined the changes of PBR in the stress/anxiety response. Dams of rats were given injection of diazepam or vehicle during puerperium. Diazepam progenies showed increased level of anxiety on the performance of elevated plus maze, and increased Bmax of PBR. Saturation experiments followed by scatchard analysis of the results showed that the increase in the density of PBR and the affinity of the PBR remained unchanged. Forced swim stress increased anxiety on the plus maze in both groups of rats. In contrast to control, diazepam progenies did not show further upregulation of renal PBR immediately after swimming stress, but still higher than control. From the above results, it may be concluded that upregulation of renal PBR is associated with chronic anxiety as well as stress-induced response.

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  8. [국내논문]   Altered Vascular Calcium Regulation in Hypertension  

    Kim, Won-Jae (Department of Physiology, Chonnam University Medical School ) , Lee, Jong-Un (Department of Physiology, Chonnam University Medical School ) , Park, Yong-Hyun (Department of Physiology, Chonnam University Medical School ) , Nam, Sang-Chae (Department of Physiology, Chonnam University Medical School)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.5 ,pp. 529 - 535 , 1997 , 1226-4512 ,

    초록

    The present study was aimed at investigating whether the vascular calcium regulation is altered in hypertension. Two-kidney, one clip (2K1C) and deoxycorticosterone acetate (DOCA)-salt hypertension were made in rats, and their thoracic aortae were taken 4 weeks later. The isometric contractile response and calcium uptake of the endothelium-denuded aortic preparations were determined. Caffeine ( $0.1{\sim}35\;mmol/L$ ) induced a greater contraction in 2K1C and DOCA-salt hypertension than in normotensive control. When the vascular calcium store was functionally-depleted by a repeated exposure to caffeine, it took longer to reload the store and to resume the initial contraction force in response to caffeine in both 2K1C and DOCA-salt hypertension. The vascular $^{45}Ca$ uptake following the functional depletion of the cellular store was also greater in both models of hypertension than in control. Ryanodine, calcium channel activator of the sarcoplasmic reticulum, attenuated the restoration of caffeine-induced vascular contraction, which was not affected by either 2K1C or DOCA-salt hypertension. Nifedipine, an L-type $Ca^{2+}$ channel blocker, attenuated the restoration of caffeine-induced contraction, which was not affected by DOCA-salt hypertension, but was more pronounced in 2K1C hypertension. Nifedipine also diminished the vascular $^{45}Ca$ uptake, which was not affected by DOCA-salt hypertension, but was more pronounced in 2K1C hypertension. Ouabain, a $Na^+,\;K^+-ATPase$ inhibitor, increased the caffeine-induced contraction by a similar magnitude in control and 2K1C hypertension, which was, however, markedly attenuated in DOCA-salt hypertension. Ouabain enhanced the vascular $^{45}Ca$ uptake, the degree of which was not affected by 2K1C hypertension, but was markedly attenuated in DOCA-salt hypertension compared with that in control. Cyclopiazonic acid, a selective inhibitor of $Ca^{2+}-ATPase$ of the sarcoplasmic reticulum, attenuated the restoration of caffeine-induced contraction, which was not affected by 2K1C hypertension, but was more marked in DOCA-salt hypertension. These results suggest that the increased vascular calcium storage may be attributed to an enhanced calcium influx in 2K1C hypertension, and to an impaired $Na^+-K^+$ pump activity of the cell membrane and subsequently increased calcium pump activity of the cellular store in DOCA-salt hypertension.

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  9. [국내논문]   Role of Intracellular Taurine in Monensin-induced $Na^+,\;Ca^{++}$ Accumulation and Mechanical Dysfunction in Isolated Rat Hearts  

    Kim, Young-Hoon (Department of Pharmacology, Seoul National University College of Medicine ) , Park, Jong-Wan (Department of Pharmacology, Seoul National University College of Medicine ) , Kim, Myung-Suk (Department of Pharmacology, 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.1 no.5 ,pp. 537 - 546 , 1997 , 1226-4512 ,

    초록

    It has been postulated that the intracellular taurine is co-transported with $Na^+$ down a concentration gradient and prevents the intracellular accumulation of sodium. It is therefore, expected that an elevated level of intracellular taurine prevents the sodium-promoted calcium influx to protect the cellular damages associated with sodium and calcium overload. In the present study, we evaluated the effects of intra- and extracellular taurine on the myocardial $Na^+$ and $Ca^{++}$ contents and the cardiac functions in isolated rat hearts which were loaded with sodium by monensin, a $Na^+-ionophore$ . Monensin caused a dose-dependent increase in intracellular $Na^+$ accompanied with a subsequent increase in intracellular $Ca^{++}$ and a mechanical dysfunction. In this monensin-treated heart, myocardial taurine content was decreased with a concomittent increase in the release of taurine. The monensin-induced increases in intracellular $Na^+$ , $Ca^{++}$ and depression of cardiac function were prevented in the hearts of which taurine content had been increased by high-taurine diet. Conversely, in the hearts of which taurine concentration gradient had been decreased by addition of taurine in the perfusate, the monensin-induced increases in $Na^+$ , $Ca^{++}$ and functional depression were accelerated. These results suggest that taurine, depending on the intra-extracellular concentration gradient, can affect intracellular sodium and calcium concentrations, and that an increased intracellular taurine may play a role in protection of myocardial dysfunction associated with the sodium and calcium overload.

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  10. [국내논문]   Role of Tyrosine Kinases in Vascular Contraction in Deoxycorticosterone Acetate-Salt Hypertensive Rats  

    Yeum, Cheol-Ho (Department of Physiology, College of Medicine, Chosun University ) , Jun, Jae-Yeoul (Department of Physiology, College of Medicine, Chosun University ) , Choi, Hyo-Sub (Department of Physiology, College of Medicine, Chosun University)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.5 ,pp. 547 - 553 , 1997 , 1226-4512 ,

    초록

    It has been known that activation of tyrosine kinases is involved in signal transduction. Role of the tyrosine kinase in vascular smooth muscle contraction was examined in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. Male Sprague-Dawley rats underwent uninephrectomy, one week after which they were subcutaneously implanted with DOCA (200 mg/kg) and supplied with 1% NaCl and 0.2% KCl drinking water for $4{\sim}6$ weeks. Control rats were treated the same except for that no DOCA was implanted. Helical strips of carotid arteries were mounted in organ baths for measurement of isometric force development. Genistein was used as a tyrosine kinase inhibitor. Concentration-response curves to 5-hydroxytryptamine (5-HT) shifted to the right by genistein in both DOCA-salt hypertensive and control rats. Although the sensitivity to genistein was similar between the two groups, the maximum force generation by 5-HT was less inhibited by genistein in arteries from DOCA-salt hypertensive rats than in those from controls. Genistein-induced relaxations were attenuated in arteries from DOCA-salt rats. Genistein affected the contraction to phorbol 12, 13-dibutyrate (PDBu) neither in DOCA-salt nor in control arteries. These observations suggest that tyrosine kinase is involved in 5-HT-induced vascular contraction, of which role is reduced in DOCA-salt hypertension.

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