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The Korean journal of physiology & pharmacology : ... 24건

  1. [국내논문]   흰쥐의 운동유발전위에 대한 전정신경핵과 연수망상핵의 역할  

    이문영 (원광대학교 의과대학 생리학교실 ) , 이성호 (원광대학교 의과대학 생리학교실 ) , 김재효 (원광대학교 의과대학 생리학교실 ) , 박병림 (원광대학교 의과대학 생리학교실 ) , 김민선 (원광대학교 의과대학 생리학교실)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.6 ,pp. 603 - 611 , 1997 , 1226-4512 ,

    초록

    The motor evoked potentials (MEPs) have been advocated as a method of monitoring the integrity of spinal efferent pathways in various injury models of the central nervous system. However, there were many disputes about origin sites of MEPs generated by transcranial electrical stimulation. The purpose of present study was to investigate the effect of major extrapyramidal motor nuclei such as lateral vestibular nucleus (VN) and medullary reticular nucleus (mRTN) on any components of the MEPs in adult Sprague-Dalwey rats. MEPs were evoked by electrical stimulation of the right sensorimotor cortex through a stainless steel screw with 0.5mm in diameter, and recorded epidurally at T9 - T10 spinal cord levels by using a pair of teflon-coated stainless steel wire electrodes with 1mm exposed tip. In order to inject lidocaine and make a lesion, insulated long dental needle with noninsulated tips were placed stareotoxically in VN and mRTN. Lidocaine of $2{\sim}3\;{\mu}l$ was injected into either VN or mRTN. The normal MEPs were composed of typical four reproducible waves; P1, P2, P3, P4. The first wave (P1) was shown at a mean latency of 1.2 ms, corresponding to a conduction velocity of 67.5 m/sec. The latencies of MEPs were shortened and the amplitudes were increased as stimulus intensity was increased. The amplitudes of P1 and P2 were more decreased among 4 waves of MEPs after lidocaine microinjection into mRTN. Especially, the amplitude of P1 was decreased by 50% after lidocaine microinjection into bilateral mRTN. On the other hand, lidocaine microinjection into VN reduced the amplitudes of P3 and P4 than other MEP waves. However, the latencies of MEPs were not changed by lidocaine microinjection into either VN or mRTN. These results suggest that the vestibular and reticular nuclei contribute to partially different role in generation of MEPs elicited by transcranial electrical stimulation.

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  2. [국내논문]   신생흰쥐 척수후근신경절 세포에서 전압의존성 $K^+$ 전류의 동정  

    김지목 (서울대학교 의과대학 생리학교실 ) , 정승준 (서울대학교 의과대학 생리학교실 ) , 김상정 (서울대학교 의과대학 생리학교실 ) , 김전 (서울대학교 의과대학 생리학교실)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.6 ,pp. 613 - 624 , 1997 , 1226-4512 ,

    초록

    Dorsal root ganglion (DRG) is composed of neuronal cell bodies of primary afferents with diverse functions. Various types of ion channels present on DRG neurons may reflect those functions. In the present study, voltage-gated potassium currents in DRG neurons of neonatal rats were characterized by whole-cell voltage clamp method. Two types of delayed rectifier and three types of transient potassium currents were identified according to their electrophysiological properties. The delayed rectifier currents were named $I_{Ke}$ (early inactivating) and $I_{K1}$ (late inactivating). Steady state inactivation of $I_{Ke}$ began from -100 mV lasting until -20 mV. $I_{K1}$ could be distinguished from $I_{Ke}$ by its inactivation voltage range, from -70 mV to +10 mV. Three transient currents were named $I_{Af}$ (fast inactivation), $I_{Ai}$ (intermediate inactivation kinetics), and $I_{As}$ (slow inactivation). $I_{Af}$ showed fast inactivation with time constant of $10.6{\pm}2.0$ msec, $I_{Ai}$ of $36.9{\pm}13.9$ msec, and $I_{As}$ of $60.6{\pm}2.9$ msec at +30 mV, respectively. They also had distinct steady state inactivation range of each. Each cell expressed diverse combination of potassium currents. The cells most frequently observed were those which expressed both $I_{K1}$ and $I_{Af}$ , and they had large diameters. The cells expressing $I_{Ke}$ and expressing $I_{Ke}$ , $I_{Ai}$ , and $I_{As}$ usually had small diameters. Judging from cell diameter, capsaicin sensitivity or action potential duration, candidates for nociceptor were the cells expressing $I_{Ke}$ , expressing $I_{Ke}$ and $I_{Ai}$ , and expressing $I_{Ke}$ and $I_{As}$ . The types and distribution of potassium currents in neonatal rat DRG were similar to those of adult rat DRG (Gold et al, 1996b).

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  3. [국내논문]   쥐 척수후각세포의 유해자극 반응에 대한 칼슘이온통로 차단제의 억제작용  

    강석한 (한양대학교 의과대학 생리학교실 및 의과학연구소 ) , 김기순 (한양대학교 의과대학 생리학교실 및 의과학연구소 ) , 신홍기 (Department of Physiology, School of Medicine, Institute of Biomedical Sciences, Hanyang University)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.6 ,pp. 625 - 637 , 1997 , 1226-4512 ,

    초록

    Calcium ions are implicated in a variety of physiological functions, including enzyme activity, membrane excitability, neurotransmitter release, and synaptic transmission, etc. Calcium antagonists have been known to be effective for the treatment of exertional angina and essential hypertension. Selective and nonselective voltage-dependent calcium channel blockers also have inhibitory action on the acute and tonic pain behaviors resulting from thermal stimulation, subcutaneous formalin injection and nerve injury. This study was undertaken to investigate the effects of iontophoretically applied $Ca^{++}$ and its antagonists on the responses of WDR (wide dynamic range) cells to sensory inputs. The responses of WDR cells to graded electrical stimulation of the afferent nerve and also to thermal stimulation of the receptive field were recorded before and after iontophoretical application of $Ca^{++}$ , EGTA, $Mn^{++}$ , verapamil, ${\omega}-conotoxin$ GVIA, ${\omega}-conotoxin$ MVIIC and ${\omega}-agatoxin$ IVA. Also studied were the effects of a few calcium antagonists on the C-fiber responses of WDR cells sensitized by subcutaneous injection of mustard oil (10%). Calcium ions and calcium channel antagonists ( $Mn^{++}$ , verapamil, ${\omega}-conotoxin$ GVIA & ${\omega}-agatoxin$ IVA) current-dependently suppressed the C-fiber responses of WDR cells without any significant effects on the A-fiber responses. But ${\omega}-conotoxin$ MVIIC did not have any inhibitory actions on the responses of WDR cell to A-fiber, C-fiber and thermal stimulation. Iontophoretically applied EGTA augmented the WDR cell responses to C-fiber and thermal stimulations while spinal application of EGTA for about $20{\sim}30\;min$ strongly inhibited the C-fiber responses. The augmenting and the inhibitory actions of EGTA were blocked by calcium ions. The WDR cell responses to thermal stimulation of the receptive field were reduced by iontophoretical application of $Ca^{++}$ , verapamil, ${\omega}-agatoxin$ IVA, and ${\omega}-conotoxin$ GVIA but not by ${\omega}-conotoxin$ MVIIC. The responses of WDR cells to C-fiber stimulation were augmented after subcutaneous injection of mustard oil (10%, 0.15 ml) into the receptive field and these sensitized C-fiber responses were strongly suppressed by iontophoretically applied $Ca^{++}$ , verapamil, ${\omega}-conotoxin$ GVIA and ${\omega}-agatoxin$ IVA. These experimental findings suggest that in the rat spinal cord, L-, N-, and P-type, but not Q-type, voltage-sensitive calcium channels are implicated in the calcium antagonist-induced inhibition of the normal and the sensitized responses of WDR cells to C-fiber and thermal stimulation, and that the suppressive effect of calcium and augmenting action of EGTA on WDR cell responses are due to changes in excitability of the cell.

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  4. [국내논문]   중추에서 혈압과 심박수 조절에 관여하는 후시상하부 콜린성 수용체의 일차적인 역할  

    김성윤 (가톨릭대학교 의과대학 약리학교실 ) , 성기욱 (가톨릭대학교 의과대학 약리학교실 ) , 고현철 (한양대학교 의과대학 약리학교실 ) , 이상복 (가톨릭대학교 의과대학 약리학교실)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.6 ,pp. 639 - 645 , 1997 , 1226-4512 ,

    초록

    The purpose of the present study is to determine the role of muscarinic cholinergic receptors of posterior hypothalamus in the central blood pressure regulation when respiration is controlled. In anesthetized and artificially ventilated rats, vasodepressor response was evoked by injection of L-glutamate(10 nmol) neuroexcitatory amino acid into the posterior hypothalamic area. The injection of $carbachol(0.5{\sim}8\;nmol)$ into the same area induced dose-dependent vasodepressor and bradycardic responses. Pretreatment with atropine(4 nmol) completely blocked the vasodepressor response to carbachol(2 nmol). In contrast, in spontaneously breathing rats, the injection of carbachol(8 nmol) into the posterior hypothalamic area induced the vasopressor and tachycardic responses. These results suggest that the muscarinic cholinergic receptors in the posterior hypothalamic area primarily play an inhibitory role in the central regulation of blood pressure and heart rate.

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  5. [국내논문]   흰쥐의 척수에서 Cyclic Nucleotides 및 Glipizide가 Baclofen의 심혈관반응에 미치는 영향  

    고현철 (한양대학교 의과대학 약리학교실 ) , 하지희 (한양대학교 의과대학 약리학교실 ) , 신인철 (한양대학교 의과대학 약리학교실)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.6 ,pp. 647 - 655 , 1997 , 1226-4512 ,

    초록

    The purpose of present study is to investigate the influence of a spinal gamma-aminobutyric acid B( $GABA_B$ ) receptor on a central regulation of blood pressure(BP) and heart rate(HR), and to define its mechanism in the spinal cord. In urethane-anesthetized, d-tubocurarine-paralyzed and artificially ventilated male Sprague-Dawley rats, intrathecal administration of drugs were carried out using injection cannula(33-gauge stainless steel) through the guide cannula(PE 10) which was inserted intrathecally at lower thoracic level through the puncture of a atlantooccipital membrane. Intrathecal injection of an $GABA_B$ receptor agonist, baclofen(30, 60, 100 nmol) decreased both BP and HR dose-dependently. Pretreatment with 8-bromo-cAMP(50 nmol), a cAMP analog, or glipizide(50 nmol), a ATP-sensitive $K^+$ channel blocker, attenuated the depressor and bradycardic effects of baclofen(100 nmol), but not with 8-bromo-cGMP(50 nmol), a cGMP analog. These results suggest that the $GABA_B$ receptor in the spinal cord plays an inhibitory role in central cardiovascular regulation and that this depressor and bradycardic actions are mediated by the decrease of cAMP via the inhibition of adenylate cyclase and the opening of $K^+$ channel.

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  6. [국내논문]   흰쥐 해마절편에서 포도당/산소 고갈에 의한 5-hydroxytryptamine 유리변동에 미치는 Adenosine의 영향  

    차광은 (이화여자대학교 의과대학 약리학교실 ) , 배영숙 (이화여자대학교 의과대학 약리학교실 ) , 이경은 (이화여자대학교 의과대학 약리학교실)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.6 ,pp. 657 - 664 , 1997 , 1226-4512 ,

    초록

    The effects of adenosine, adenosine A1 receptor antagonist (DPCPX), or NMDA receptor antagonist (APV) on the spontaneous release of $[^3H]-5-hydroxytryptamine$ ( $[^3H]-5-HT$ ) during normoxic/normoglycemic or hypoxic/hypoglycemic period were studied in the rat hippocampal slices. The hippocampus was obtained from the rat brain and sliced $400\;{\mu}m$ thickness with the tissue slicer. After 30 min's preincubation in the normal buffer, the slices were incubated for 30 min in a buffer containing $[^3H]-5-HT$ ( $0.1\;{\mu}M,\;74{\mu}Ci/8\;ml$ ) for uptake, and washed. To measure the release of $[^3H]-5-HT$ into the buffer, the incubation medium was drained off and refilled every ten minutes through sequence of 14 tubes. Induction of glucose/oxygen deprivation (GOD; medium depleting glucose and gassed with 95% $N_2/5%\;CO_2$ ) was done in 6th and 7th tube. The radioactivities in each buffer and the tissue were counted using liquid scintillation counter and the results were expressed as a percentage of the total radioactivities. When slices were exposed to GOD for 20 mins, the spontaneous release of $[^3H]-5-HT$ was markedly increased and this increase of $[^3H]-5-HT$ release was blocked by adenosine ( $10\;{\mu}M$ ) or DL-2-amino-5-phosphonovaleric acid (APV; $30\;{\mu}M$ ). Adenosine $A_1$ receptor specific antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX) exacerbate GOD-induced increase of spontaneous release of $[^3H]-5-HT$ . These results suggest that Adenosine may play a role in the GOD-induced spontaneous release of $[^3H]-5-HT$ through adenosine $A_1$ receptor activity.

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  7. [국내논문]   PAF 길항제가 허혈성 대뇌 피질내 Nitric Oxide 합성에 미치는 영향  

    노순기 (봉생병원 신경과 ) , 박규현 (부산대학교 의과대학 신경과학교실 ) , 이원석 (부산대학교 의과대학 약리학교실)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.6 ,pp. 665 - 672 , 1997 , 1226-4512 ,

    초록

    This study aimed to investigate the mechanism of cerebroprotection of platelet-activating factor(PAF) antagonists in transient cerebral ischemia of rat. Right middle cerebral artery(MCA) of Sprague-Dawley rat was occluded for 2 hours using an intraluminal filament technique. After 22 hours of reperfusion, morphometrically detectable infarct was developed in the cortex and striatum identical to the territory of MCA. The infarct size was significantly reduced by PAF antagonists, BN 52021 and CV-6209, as well as an inducible nitric oxide synthase(iNOS) inhibitor aminoguanidine(1 mg/kg, i.p., respectively) administered 5 min after MCA occlusion. PAF antagonists significantly inhibited the enzymatic activities of both myeloperoxidase and iNOS in the cerebral hemisphere ipsilateral to ischemia, whereas aminoguanidine did not inhibit myeloperoxidase activity but significantly inhibited the iNOS activity. These results suggest that PAF antagonists exert a cerebroprotective effect against ischemic brain damage through inhibition of leukocyte infiltration and iNOS activity in the postischemic brain.

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  8. [국내논문]   흰쥐 대뇌피질 절편에서 허혈에 의한 Norepinephrine 유리에 있어서 Nitric Oxide의 영향  

    은영아 (전북대학교 의과대학 약리학교실, 전북대학교 의과학연구소 ) , 김동찬 (전북대학교 의과대학 마취과학교실, 전북대학교 의과학연구소 ) , 조규박 (전북대학교 의과대학 약리학교실, 전북대학교 의과학연구소 ) , 김기원 (전북대학교 의과대학 약리학교실, 전북대학교 의과학연구소)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.6 ,pp. 673 - 679 , 1997 , 1226-4512 ,

    초록

    It has been generally accepted that glutamate mediates the ischemic brain damage, excitotoxicity, and induces release of neurotransmitters, including norepinephrine(NE), in ischemic milieu. In the present study, the role of nitric oxide(NO) in the ischemia-induced $[^3H]norepinephrine([^3H]NE)$ release from cortex slices of the rat was examined. Ischemia, deprivation of oxygen and glucose from $Mg^{2+}-free$ artificial cerebrospinal fluid, induced significant release of $[^3H]NE$ from cortex slices. This ischemia-induced $[^3H]NE$ release was significantly attenuated by glutamatergic neurotransmission modifiers. $N^G-nitro-L-arginine$ methyl ester(L-NAME), $N^G-monomethyl-L-arginine$ (L-NMMA) or 7-nitroindazole, nitric oxide synthase inhibitors attenuated the ischemia-evoked $[^3H]NE$ release. Hemoglobin, a NO chelator, and 5, 5- dimethyl-L-pyrroline-N-oxide(DMPO), an electron spin trap, inhibited $[^3H]NE$ release dose-dependently. Ischemia-evoked $[^3H]NE$ release was inhibited by methylene blue, a soluble guanylate cyclase inhibitor, and potentiated by 8-bromo-cGMP, a cell permeable cGMP analog, zaprinast, a cGMP phosphodiesterase inhibitor, and S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide generator. These results suggest that the ischemia-evoked $[^3H]NE$ release is mediated by NMDA receptors, and activation of NO system is involved.

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  9. [국내논문]   해마절편의 허혈성 $K^+$ 축적에 대한 $K^+$채널 조절 약물의 작용  

    최진규 (서울대학교 수의과대학 약리학교실 ) , 전보권 (고려대학교 의과대학 약리학교실 ) , 류판동 (서울대학교 수의과대학 약리학교실)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.6 ,pp. 681 - 690 , 1997 , 1226-4512 ,

    초록

    Loss of synaptic transmission and accumulation of extracellular $K^+([K^+]_O)$ are the key features in ischemic brain damage. Here, we examined the effects of several $K^+$ channel modulators on the early ischemic changes in population spike (PS) and $[K^+]_o$ in the CA1 pyramidal layer of the rat hippocampal slice using electrophysiological techniques. After onset of anoxic aglycemia (AA), orthodromic field potentials decreased and disappeared in $3.3{\pm}0.22\;min$ $(mean{\pm}SEM,\;n=40)$ . The hypoxic injury potential (HIP), a transient recovery of PS appeared at $6.0{\pm}0.25\;min$ (n=40) in most slices during AA and lasted for $3.3{\pm}0.43\;min$ . $[K^+]_o$ increased initially at a rate of 0.43 mM/min (Phase 1) and later at a much faster rate (12.45 mM/min, Phase 2). The beginning of Phase 2 was invariably coincided with the disappearance of HIP. Among $K^+$ channel modulators tested such as 4-aminopyridine (0.03, 0.3 mM), tetraethylammonium (0.1 mM), NS1619 $(0.3{\sim}10\;{\mu}M)$ , niflumic acid (0.1 mM), glibenclamide $(40\;{\mu}M)$ , tolbutamide $(300\;{\mu}M)$ and pinacidil $(100\;{\mu}M)$ , only 4-aminopyridine (0.3 mM) induced slight increase of $[K^+]_o$ during Phase 1. However, none of the above agents modulated the pattern of Phase 2 in $[K^+]_o$ in response to AA. Taken together, the experimental data suggest that 4-aminopyridine-sensitive $K^+$ channels, large conductance $Ca^{2+}-activated$ $K^+$ channels and ATP-sensitive $K^+$ channels may not be the major contributors to the sudden increase of $[K^+]_o$ during the early stage of brain ischemia, suggesting the presence of other routes of $K^+$ efflux during brain ischemia.

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  10. [국내논문]   사람 Neuroblastoma SH-SY5Y 세포주에서 Opiate 내성에 의한 c-myc 유전자 표현  

    박창교 (계명대학교 의과대학 약리학교실 및 의과학연구소 ) , 권지윤 (계명대학교 의과대학 약리학교실 및 의과학연구소 ) , 서성일 (계명대학교 의과대학 미생물학교실 및 의과학연구소 ) , 김수경 (계명대학교 의과대학 약리학교실 및 의과학연구소)
    The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology v.1 no.6 ,pp. 691 - 697 , 1997 , 1226-4512 ,

    초록

    The mechanisms underlying opiate tolerance and dependence are not fully understood. We used human neuroblastoma SH-SY5Y cells as a model system for studying effects of morphine tolerance and withdrawal on c-myc induction and cAMP levels. It has been reported that regulation of c-fos by acute and chronic morphine withdrawal is mediated through alterations in CREB transcription factor. In this study, we examined the effects of morphine tolerance on c-myc expression and cAMP concentrations. The activation of opiate receptors by an acute morphine administration resulted in an increase in c-myc mRNA and a decrease in cAMP concentrations in a dose-dependent manner $(5,\;10,\;15,\;and\;20\;{\mu}M)$ . On the other hand, the chronic treatment of morphine $(10\;{\mu}M\;for\;six\;days)$ did not induce the elevated expression of c-myc mRNA. The c-myc expression was slightly inhibited in comparison with that of the acute morphine response. However, cAMP concentrations were increased with regard to morphine withdrawal response. These results suggest that the alterations in c-myc expression might imply a significant opiate regulation relating to morphine tolerance. This observation differs from increased expression of c-fos via regulation of cAMP pathway.

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