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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 蔡明正(Ming-Cheng Tsai) | |
dc.contributor.author | Guan-Ling Lu | en |
dc.contributor.author | 盧冠伶 | zh_TW |
dc.date.accessioned | 2021-06-13T04:17:53Z | - |
dc.date.available | 2007-08-02 | |
dc.date.copyright | 2006-08-02 | |
dc.date.issued | 2006 | |
dc.date.submitted | 2006-07-24 | |
dc.identifier.citation | Aarts,M.M. and Tymianski,M. (2004). Molecular mechanisms underlying specificity of excitotoxic signaling in neurons. Curr. Mol. Med. 4, 137-147.
Afshari,F.S., Ptak,K., Khaliq,Z.M., Grieco,T.M., Slater,N.T., McCrimmon,D.R., and Raman,I.M. (2004). Resurgent Na currents in four classes of neurons of the cerebellum. J. Neurophysiol. 92, 2831-2843. Arvanov,V.L., Liou,H.H., Chang,Y.C., Chen,R.C., Peng,F.C., Ling,K.H., and Tsai,M.C. (1994). Interactions of anticholinesterases with Achatina fulica acetylcholine responses and electrogenic sodium pump. Neuroscience 62, 581-586. Bao,L., Avshalumov,M.V., and Rice,M.E. (2005). Partial mitochondrial inhibition causes striatal dopamine release suppression and medium spiny neuron depolarization via H2O2 elevation, not ATP depletion. J. Neurosci. 25, 10029-10040. Bourque,C.W. and Renaud,L.P. (1985). Calcium-dependent action potentials in rat supraoptic neurosecretory neurones recorded in vitro. J. Physiol 363, 419-428. Brown,A.M., Brodwick,M.S., and Eaton,D.C. (1977). Intracellular calcium and extra-retinal photoreception of Aplysia Giant neurons. J. Neurobiol. 8, 1-18. Bruno,V., Scapagnini,U., and Canonico,P.L. (1993). Excitatory amino acids and neurotoxicity. Funct. Neurol. 8, 279-292. Cahalan,M.D. and Almers,W. (1979). Interactions between quaternary lidocaine the sodium channel gates, and tetrodotoxin. Biophys. J. 27, 39-55. Chang,S. and Lamm,S.H. (2003). Human health effects of sodium azide exposure: a literature review and analysis. Int. J. Toxicol. 22, 175-186. Chen,Y.H., Chang,C.H., Liang,G.J., Huang,S.S., Hsieh,H.M., Teng,C.M., and Tsai,M.C. (2000). Burst firing of action potentials in central snail neurons elicited by d-amphetamine: effect of anticonvulsants. Comp Biochem. Physiol C. Toxicol. Pharmacol. 127, 221-231. Chen,Y.H., Lin,C.H., Lin,P.L., and Tsai,M.C. (2006). Cocaine elicits action potential bursts in a central snail neuron: the role of delayed rectifying K+ current. Neuroscience 138, 257-280. Chen,Y.H. and Tsai,M.C. (1997). Bursting firing of action potentials in central snail neurons elicited by d-amphetamine: role of cytoplasmic second messengers. Neurosci. Res. 27, 295-304. Chen,Y.H. and Tsai,M.C. (2000). Action potential bursts in central snail neurons elicited by d-amphetamine: roles of ionic currents. Neuroscience 96, 237-248. Chen,Y. and Tsai,M. (1996). Bursting firing of action potential in central snail neuron elicited by d-amphetamine: role of the intracellular calcium ions. Comp Biochem. Physiol. A 115, 195-205. Cock,H.R. (2002). The role of mitochondria and oxidative stress in neuronal damage after brief and prolonged seizures. Prog. Brain Res. 135, 187-196. Derlet,R.W., Albertson,T.E., and Rice,P. (1990a). Antagonism of cocaine, amphetamine, and methamphetamine toxicity. Pharmacol. Biochem. Behav. 36, 745-749. Derlet,R.W., Albertson,T.E., and Rice,P. (1990b). Protection against d-amphetamine toxicity. Am. J. Emerg. Med. 8, 105-108. Derlet,R.W., Albertson,T.E., and Rice,P. (1990c). The effect of SCH 23390 against toxic doses of cocaine, d-amphetamine and methamphetamine. Life Sci. 47, 821-827. Ferguson,M., Mockett,R.J., Shen,Y., Orr,W.C., and Sohal,R.S. (2005). Age-associated decline in mitochondrial respiration and electron transport in Drosophila melanogaster. Biochem. J. 390, 501-511. Hasham,M.I., Naumann,D., Kim,S.U., Cashman,N.R., Quamme,G.A., and Krieger,C. (1994). Intracellular calcium concentrations during metabolic inhibition in the motoneuron cell line NSC-19. Can. J. Physiol Pharmacol. 72, 728-737. Hehl,S., Golard,A., and Hille,B. (1996). Involvement of mitochondria in intracellular calcium sequestration by rat gonadotropes. Cell Calcium 20, 515-524. Heinemann,U., Buchheim,K., Gabriel,S., Kann,O., Kovacs,R., and Schuchmann,S. (2002). Cell death and metabolic activity during epileptiform discharges and status epilepticus in the hippocampus. Prog. Brain Res. 135, 197-210. Higashima,M., Ohno,K., and Koshino,Y. (2002). Cyclic AMP-mediated modulation of epileptiform afterdischarge generation in rat hippocampal slices. Brain Res. 949, 157-161. Hodgkin,A.L. and Keynes,R.D. (1955). The potassium permeability of a giant nerve fibre. J. Physiol 128, 61-88. Hrudka,F. (1987). Cytochemical and ultracytochemical demonstration of cytochrome c oxidase in spermatozoa and dynamics of its changes accompanying ageing or induced by stress. Int. J. Androl 10, 809-828. Inoue,I. (1980). Separation of the action potential into a Na-channel spike and a K-channel spike by tetrodotoxin and by tetraethylammonium ion in squid giant axons internally perfused with dilute Na-salt solutions. J. Gen. Physiol 76, 337-354. Jerelova,O.M., Krasts,I.V., and Veprintsev,B.N. (1971). The effect of sodium, calcium and magnesium on the amplitude of the action potential from giant neurons of Limnaea stagnalis. Comp Biochem. Physiol A 40, 281-293. Jin,W., Sugaya,A., Tsuda,T., Ohguchi,H., and Sugaya,E. (2000). Relationship between large conductance calcium-activated potassium channel and bursting activity. Brain Res. 860, 21-28. Kerkut,G.A., Lambert,J.D., Gayton,R.J., Loker,J.E., and Walder,R.J. (1975). Mapping of nerve cells in the suboesophageal ganglia of Helix aspersa. Comp Biochem. Physiol A 50, 1-25. Kramer,R.H. and Zucker,R.S. (1985). Calcium-dependent inward current in Aplysia bursting pace-maker neurones. J. Physiol 362, 107-130. Kunimoto,S., Nosaka,C., and Takeuchi,T. (1999). Stimulation of cellular XTT reduction by cytochrome oxidase inhibitors. Biol. Pharm. Bull. 22, 660-661. Kunz,W.S. (2002). The role of mitochondria in epileptogenesis. Curr. Opin. Neurol. 15, 179-184. Lee,W.T., Yin,H.S., and Shen,Y.Z. (2002). The mechanisms of neuronal death produced by mitochondrial toxin 3-nitropropionic acid: the roles of N-methyl-D-aspartate glutamate receptors and mitochondrial calcium overload. Neuroscience 112, 707-716. Lewis,D.V. (1984). Spike aftercurrents in R15 of Aplysia: their relationship to slow inward current and calcium influx. J. Neurophysiol. 51, 387-403. Lewis,D.V. (1988). Calcium-activated inward spike after-currents in bursting neurone R15 of Aplysia. J. Physiol 395, 285-302. Lewis,D.V. and Wilson,W.A. (1982). Calcium influx and poststimulus current during early adaptation in Aplysia giant neurons. J. Neurophysiol. 48, 202-216. Lin,C.H., Lin,P.J., Chen,Y.H., Lin,P.L., Chen,I.M., Lu,K.L., Chang,Y.C., and Tsai,M.C. (2005). Effects of rolipram on induction of action potential bursts in central snail neurons. Exp. Neurol. 194, 384-392. Lin,C.H., Liu,M.C., Lin,M.S., Lin,P.L., Chen,Y.H., Chen,C.T., Chen,I.M., and Tsai,M.C. (2005). Effects of a new isoquinolinone derivative on induction of action potential bursts in central snail neuron. Pharmacology 75, 98-110. Lin,C.H. and Tsai,M.C. (2003). D-amphetamine-elicited action potential bursts in central snail neurons: role of second messenger systems. J. Formos. Med. Assoc. 102, 394-403. Lin,C.H. and Tsai,M.C. (2005a). Effects of procaine on a central neuron of the snail, Achatina fulica Ferussac. Life Sci. 76, 1641-1666. Lin,C.H. and Tsai,M.C. (2005b). The modulation effects of d-amphetamine and procaine on the spontaneously generated action potentials in the central neuron of snail, Achatina fulica Ferussac. Comp Biochem. Physiol C. Toxicol. Pharmacol. 141, 58-68. Lin,C.H., Wu,C.L., Lin,M.S., Liu,M.C., Lin,P.J., and Tsai,M.C. (2005). Effects of 2,3-butanedione monoxime on induction of action potential bursts in central snail neurons: direct and indirect modulations of ionic currents. Pharmacology 73, 57-69. Lux,H.D. (1976). Change of potassium activity associated with membrane current flow. Fed. Proc. 35, 1248-1253. Maue,R.A. and Dionne,V.E. (1987). Patch-clamp studies of isolated mouse olfactory receptor neurons. J. Gen. Physiol 90, 95-125. McClintock,T.S. and Ache,B.W. (1989). Ionic currents and ion channels of lobster olfactory receptor neurons. J. Gen. Physiol 94, 1085-1099. Meldolesi,J., Villa,A., Podini,P., Clementi,E., Zacchetti,D., D'Andrea,P., Lorenzon,P., and Grohovaz,F. (1992). Intracellular Ca2+ stores in neurons. Identification and functional aspects. J. Physiol Paris 86, 23-30. Miczek,K.A. and Weerts,E.M. (1987). Seizures in drug-treated animals. Science 235, 1127-1128. Mironov,S.L. and Richter,D.W. (1999). Cytoskeleton mediates inhibition of the fast Na+ current in respiratory brainstem neurons during hypoxia. Eur. J. Neurosci. 11, 1831-1834. Moffatt,E.J. and Miyamoto,M.D. (1988). Effect of sodium and calcium channel blockade on the increase in spontaneous transmitter release produced by the mitochondrial inhibitor, dinitrophenol. J. Pharmacol. Exp. Ther. 244, 613-618. Nicholls,D.G. (2006). Simultaneous monitoring of ionophore- and inhibitor-mediated plasma and mitochondrial membrane potential changes in cultured neurons. J. Biol. Chem. 281, 14864-14874. O'Day,P.M., Bacigalupo,J., Vergara,C., and Haab,J.E. (1997). Current issues in invertebrate phototransduction. Second messengers and ion conductances. Mol. Neurobiol. 15, 41-63. Ohmori,H. (1984). Studies of ionic currents in the isolated vestibular hair cell of the chick. J. Physiol 350, 561-581. Onozuka,M., Imai,S., and Ozono,S. (1990). The 70-kDa epileptic cortical protein elicits bursting activity accompanied by a reduction of outward current in Euhadra neurons which is inhibited by an antibody against this protein. Brain Res. 531, 276-279. Onozuka,M., Kubo,K.Y., and Ozono,S. (1991). The molecular mechanism underlying pentylenetetrazole-induced bursting activity in Euhadra neurons: involvement of protein phosphorylation. Comp Biochem. Physiol C. 100, 423-432. Palmer,G. (1993). Current issues in the chemistry of cytochrome c oxidase. J. Bioenerg. Biomembr. 25, 145-151. Patel,M. (2004). Mitochondrial dysfunction and oxidative stress: cause and consequence of epileptic seizures. Free Radic. Biol. Med. 37, 1951-1962. Penner,R., Matthews,G., and Neher,E. (1988). Regulation of calcium influx by second messengers in rat mast cells. Nature 334, 499-504. Platel,J.C., Boisseau,S., Dupuis,A., Brocard,J., Poupard,A., Savasta,M., Villaz,M., and Albrieux,M. (2005). Na+ channel-mediated Ca2+ entry leads to glutamate secretion in mouse neocortical preplate. Proc. Natl. Acad. Sci. U. S. A 102, 19174-19179. Pontzer,N.J., Chandler,L.J., Stevens,B.R., and Crews,F.T. (1990). Receptors, phosphoinositol hydrolysis and plasticity of nerve cells. Prog. Brain Res. 86, 221-225. Raeymaekers,L., Wuytack,F., Batra,S., and Casteels,R. (1977). A comparative study of the calcium accumulation by mitochondria and microsomes isolated from the smooth muscle of the guinea-pig taenia coli. Pflugers Arch. 368, 217-223. Sanchez,J.C., Mareci,T.H., Norman,W.M., Principe,J.C., Ditto,W.L., and Carney,P.R. (2006). Evolving into epilepsy: Multiscale electrophysiological analysis and imaging in an animal model. Exp. Neurol. 198, 31-47. Sawaki,K. and Kawaguchi,M. (1989). Some correlations between procaine-induced convulsions and monoamines in the spinal cord of rats. Jpn. J. Pharmacol. 51, 369-376. Sawaki,K., Ohno,K., Miyamoto,K., Hirai,S., Yazaki,K., and Kawaguchi,M. (2000). Effects of anticonvulsants on local anaesthetic-induced neurotoxicity in rats. Pharmacol. Toxicol. 86, 59-62. Sawaki,K., Ouchi,K., Sato,T., and Kawaguchi,M. (1991). Some correlations between local anesthetic-induced convulsions and gamma-aminobutyric acid in rat spinal cord. Jpn. J. Pharmacol. 56, 327-335. Scholz,K.P. and Byrne,J.H. (1988). Intracellular injection of cAMP induces a long-term reduction of neuronal K+ currents. Science 240, 1664-1666. Schwartzkroin,P.A. (1994). Cellular electrophysiology of human epilepsy. Epilepsy Res. 17, 185-192. Seo,B.B., Nakamaru-Ogiso,E., Flotte,T.R., Yagi,T., and Matsuno-Yagi,A. (2002). A single-subunit NADH-quinone oxidoreductase renders resistance to mammalian nerve cells against complex I inhibition. Mol. Ther. 6, 336-341. Simon,D.K. and Johns,D.R. (1999). Mitochondrial disorders: clinical and genetic features. Annu. Rev. Med. 50, 111-127. Stout,M.A., Diecke,F.P., and Greenberg,S. (1980). Effect of metabolic inhibitors on 45Ca fluxes and ATP content of myelinated nerve. Arch. Int. Pharmacodyn. Ther. 243, 292-303. Sugaya,E., Furuichi,H., Takagi,T., Kajiwara,K., and Komatsubara,J. (1987). Intracellular calcium concentration during pentylenetetrazol-induced bursting activity in snail neurons. Brain Res. 416, 183-186. Sugaya,E. and Onozuka,M. (1978). Intracellular calcium: its movement during pentylenetetrazole-induced bursting activity. Science 200, 797-799. Sun,X.P. and Takeuchi,H. (1986). Decreases of action potential amplitudes, in sodium-free and calcium-free conditions, of identifiable giant neurons of an African giant snail (Achatina fulica Ferussac)--I. The right parietal ganglion. Comp Biochem. Physiol A 84, 19-24. Takeuchi,H., Araki,Y., Emaduddin,M., Zhang,W., Han,X.Y., Salunga,T.L., and Wong,S.M. (1996). Identifiable Achatina giant neurones: their localizations in ganglia, axonal pathways and pharmacological features. Gen. Pharmacol. 27, 3-32. Taylor,C.W. and Marshall,I.C. (1992). Calcium and inositol 1,4,5-trisphosphate receptors: a complex relationship. Trends Biochem. Sci. 17, 403-407. Tillotson,D. and Gorman,A.L. (1980). Non-uniform Ca2+ buffer distribution in a nerve cell body. Nature 286, 816-817. Tirosh,O., Sen,C.K., Roy,S., and Packer,L. (2000). Cellular and mitochondrial changes in glutamate-induced HT4 neuronal cell death. Neuroscience 97, 531-541. Tsai,M.C. (1986). The ionic requirements for the production of action potential in Achatina fulica Ferussac neuron. Proc. Natl. Sci. Counc. Repub. China B 10, 269-274. Tsai,M.C. and Chen,Y.H. (1995). Bursting firing of action potentials in central snail neurons elicited by d-amphetamine: role of the electrogenic sodium pump. Comp Biochem. Physiol C. Pharmacol. Toxicol. Endocrinol. 111, 131-141. Tsien,R.Y. and Zucker,R.S. (1986). Control of cytoplasmic calcium with photolabile tetracarboxylate 2-nitrobenzhydrol chelators. Biophys. J. 50, 843-853. Urbanska,E.M. (2000). Seizures evoked by mitochondrial toxin, 3-nitropropionic acid: new mechanism of epileptogenesis? Pol. J. Pharmacol. 52, 55-57. Urbanska,E.M., Blaszczak,P., Saran,T., Kleinrok,Z., and Turski,W.A. (1998). Mitochondrial toxin 3-nitropropionic acid evokes seizures in mice. Eur. J. Pharmacol. 359, 55-58. Verkhratsky,A. and Shmigol,A. (1996). Calcium-induced calcium release in neurones. Cell Calcium 19, 1-14. Wasterlain,C.G., Niquet,J., Thompson,K.W., Baldwin,R., Liu,H., Sankar,R., Mazarati,A.M., Naylor,D., Katsumori,H., Suchomelova,L., and Shirasaka,Y. (2002). Seizure-induced neuronal death in the immature brain. Prog. Brain Res. 135, 335-353. Watanabe,K. and Funase,K. (1991). Cyclic AMP elicits biphasic current whose activation is mediated through protein phosphorylation in snail neurons. Neurosci. Res. 10, 64-70. Waters,S.L., Wong,J.K., and Schnellmann,R.G. (1997). Depletion of endoplasmic reticulum calcium stores protects against hypoxia- and mitochondrial inhibitor-induced cellular injury and death. Biochem. Biophys. Res. Commun. 240, 57-60. Yamamoto,H. (1990). Protection against cyanide-induced convulsions with alpha-ketoglutarate. Toxicology 61, 221-228. Yamamoto,H. and Tang,H.W. (1996). Preventive effect of melatonin against cyanide-induced seizures and lipid peroxidation in mice. Neurosci. Lett. 207, 89-92. Zuchora,B. and Urbanska,E.M. (2001). Effect of adenosine receptor agonists on neurodegenerative and convulsive activity of mitochondrial toxin, 3-nitropropionic acid. Pol. J. Pharmacol. 53, 69-71. | |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/32876 | - |
dc.description.abstract | 1.本論文主要探討代謝性抑制劑 (metabolic inhibitors, NaN3、rotenone及KCN) 對於非洲大蝸牛 (Achatina fulica) 之RP4神經元之 (1) 自發性動作電位的影響; (2) d-amphetamine引發RP4神經元產生猝發現象之相關性。
2.正常生理溶液灌流下,RP4神經元會產生規律的自發性動作電位(spontaneous action potential)。當投予低濃度的代謝性抑制劑 NaN3 (30、100、300 μM、1及3 mM)、rotenone (3、10及30 μM)及KCN (0.3、1 及3 mM) 經灌流60分鐘後,對RP4神經元的自發性動作電位並無影響。 3.當投予高濃度的代謝性抑制劑 NaN3 (30 mM) 20分鐘、rotenone (100 μM) 10分鐘及KCN (10 mM) 10分鐘後,RP4神經元的自發性動作電位會被抑制且靜止膜電位有去極化的現象。 4.NaN3 (30 mM) 會使RP4神經元自發性動作電位逐漸消失且有去極化的現象。利用電流箝制 (current clamp) 的方法給予一個過極化的電流後,可以觀察到動作電位有部分恢復的現象,表示NaN3 (30 mM) 導致RP4神經元之自發性動作電位消失與去極化有關。 5.高濃度的NaN3 (30 mM) 會使RP4神經元自發性動作電位的振幅逐漸消失。利用膜電位箝制 (voltage clamp) 發現高濃度的NaN3 (10及30 mM) 會減少RP4神經元之總內向電流,推論此總內向電流的減少與RP4神經元自發性動作電位的振幅逐漸消失有關。為了了解低濃度的NaN3 (30 μM) 是否經由影響離子電流來促進低濃度的d-amphetamine (135 μM) 產生猝發現象。利用膜電位箝制 (voltage clamp) 發現NaN3 (30 μM) 對總內向及總外向電流的影響皆不顯著。顯示NaN3 在30 μM時,並不經由離子電流的改變來促進低濃度d-amphetamine (135 μM) 產生猝發現象。 6.NaN3 (10及30 mM) 對RP4神經元input resistance的影響並不顯著;且NaN3 (10及30 mM) 對總外向電流的影響也不顯著,表示NaN3 (10及30 mM) 對RP4神經元細胞膜鉀離子的permeability無顯著之影響。 7.投予較低濃度之d-amphetamine (135 μM) 60分鐘後,不會引起RP4神經元產生猝發性動作電位,然而若投予較高濃度的d-amphetamine (270 μM) 經30分鐘,即可誘發猝發現象產生。顯示d-amphetamine引起的猝發性動作電位具有濃度依賴性。 8.使用低濃度的代謝性抑制劑NaN3 (30 μM)、rotenone (10 μM) 及KCN (1 mM) 灌流60分鐘後,再給予較低濃度的d-amphetamine (135 μM) 60分鐘,則RP4神經元會產生猝發性動作電位。結果顯示低濃度的代謝性抑制劑有促進低濃度的d-amphetamine (135 μM) 產生猝發性動作電位的能力。 9.使用低濃度的代謝性抑制劑 NaN3 (30 μM)、rotenone (10 μM) 及KCN (1 mM) 灌流60分鐘後,再給予較低濃度的procaine (5 mM) 60分鐘,則RP4神經元會產生猝發性動作電位。結果顯示低濃度的代謝性抑制劑有促進低濃度的procaine (5 mM) 產生猝發性動作電位的能力。 10.若以KT5720 (10 μM) 灌流RP4神經元60分鐘,再加入 NaN3 (30 μM) 60分鐘及d-amphetamine (135 μM) 60分鐘後,RP4神經元無猝發現象產生。此結果顯示KT5720 (10 μM) 可以抑制NaN3 (30 μM) 促進低濃度的d-amphetamine (135 μM) 產生猝發性動作電位,所以經NaN3 (30 μM) 促進低濃度的d-amphetamine (135 μM)產生猝發性動作電位的現象,極有可能與cAMP-dependent protein kinase system的路徑有關。 11.預先以NaN3 (30 μM) 促進低濃度的d-amphetamine (135 μM) 產生猝發性動作電位後,接著投予phospholipase C抑制劑U73122 (10 | zh_TW |
dc.description.abstract | The roles of metabolic inhibitors (including NaN3, rotenone and KCN) on (1) spontaneous action potential and (2) bursts of potential elicited by d-amphetamine were studied on RP4 neurons of snail, Achatina fulica Ferussac in vitro.
Metabolic inhibitors altered the spontaneous action potential in a concentration dependant manner. Lower concentrations of NaN3 (30, 100, 300 μM, 1 and 3 mM), rotenone (3, 10 and 30 μM) and KCN (0.3, 1 and 3 mM), did not affect the resting membrane potential, amplitude and frequency on RP4 neurons, while higher concentrations of NaN3 (30 mM), rotenone (100 μM) and KCN (10 mM) did abolish the spontaneous action potential on RP4 neurons and depolarize the RP4 neurons. The action potential was partially recovered that if injected a hyperpolarized current into the depolarized RP4 neurons. NaN3 (10 and 30 mM) did not alter the input resistance of the RP4 neurons. Voltage clamp studies revealed that NaN3 (10 and 30 mM) decreased the total fast inward currents (70 ms) while the steady-state outward currents (5 s) were not altered. These results suggested that NaN3 (10 and 30 mM) abolished the spontaneous action potential on RP4 neurons by depolarizing RP4 neurons and decreasing the total fast inward currents, while the input resistance and the permeability of potassium ion on RP4 neurons were not involved. Interactions between metabolic inhibitors and d-amphetamine or procaine were studied. No bursts of potential were found 60 min after administration of d-amphetamine (135 μM) or 120 min after administration of metabolic inhibitors, NaN3 (30 μM), rotenone (10 μM) or KCN (1 mM) on RP4 neurons. However, bursts of potential were found 60 min after d-amphetamine (135 μM) administration if NaN3 (30 μM), rotenone (10 μM) or KCN (1 mM) was treated 60 min prior to d-amphetamine administration. No burst of potential was found 60 min after administration of procaine (5 mM) on RP4 neurons. However, bursts of potential were found 60 min after procaine (5 mM) administration if NaN3 (30 μM), rotenone (10 μM) or KCN (1 mM) was treated 60 min prior to procaine administration. These results suggested that lower concentrations of metabolic inhibitors could facilitate the bursts elicited by d-amphetamine (135 μM) or procaine (5 mM). The bursts of potential elicited by NaN3 (30 μM) and d-amphetamine (135 μM) decreased following treatment with KT5720 (protein kinase A inhibitors) or intracellular injection of EGTA. However, the bursts of potential were not affected by applying U73122 or neomycin (phospolipase inhibitors). Voltage clamp studies revealed that NaN3 (30 μM) didn’t significantly alter total fast inward and steady-state outward currents. These results suggested that the bursting activity elicited by NaN3 (30 μM) and d-amphetamine (135 μM) was mainly due to PKA related messenger system and intracellular calcium, while phospholipase activity and change of ion current were not involved. It is concluded that metabolic inhibitors abolished the spontaneous action potential on the RP4 neurons. The effect was associated with depolarizing RP4 neurons and decrease of fast total inward currents, while it was not associated with input resistance and the permeability of potassium ion on RP4 neurons. The lower concentrations of metabolic inhibitors could facilitate the bursts of potential elicited by lower concentrations of d-amphetamine and procaine. The effect of NaN3 and d-amphetamine may be related to PKA and intracellular calcium, while it was not related to phospholipase and change of ion currents. | en |
dc.description.provenance | Made available in DSpace on 2021-06-13T04:17:53Z (GMT). No. of bitstreams: 1 ntu-95-R93443013-1.pdf: 2634189 bytes, checksum: bd348cd3a23f62cf5b0577e528fc8254 (MD5) Previous issue date: 2006 | en |
dc.description.tableofcontents | 一、縮寫表 ( Abbreviation ) ii
二、中文摘要( Abstract in Chinese ) 1 三、英文摘要( Abstract in English ) 5 四、緒論 (Introduction ) 7 五、實驗方法與材料( Materials and Methods ) 11 六、實驗結果 ( Results ) 15 七、討論與結論( Discussion and Conclusion ) 32 八、參考文獻( References ) 41 九、圖表 ( Figures and Tables ) 48 | |
dc.language.iso | zh-TW | |
dc.title | 代謝性抑制劑對安非他命及普卡因引起之猝發動作電位影響之研究 | zh_TW |
dc.title | Effects of metabolic inhibitors on the potential changes elicited by d-amphetamine and procaine | en |
dc.type | Thesis | |
dc.date.schoolyear | 94-2 | |
dc.description.degree | 碩士 | |
dc.contributor.oralexamcommittee | 邱蔡賢(Tsai-Hsien Chiu),林滿玉(Mann-Yuh Lin) | |
dc.subject.keyword | 代謝性抑制劑,安非他命,猝發現象, | zh_TW |
dc.subject.keyword | metabolic inhibitor,d-amphetamine,bursting, | en |
dc.relation.page | 80 | |
dc.rights.note | 有償授權 | |
dc.date.accepted | 2006-07-25 | |
dc.contributor.author-college | 醫學院 | zh_TW |
dc.contributor.author-dept | 藥理學研究所 | zh_TW |
顯示於系所單位: | 藥理學科所 |
文件中的檔案:
檔案 | 大小 | 格式 | |
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ntu-95-1.pdf 目前未授權公開取用 | 2.57 MB | Adobe PDF |
系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。