請用此 Handle URI 來引用此文件:
http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/56365完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 尹相姝(Hsiang-Shu Yin) | |
| dc.contributor.author | Chuan-Ching Lai | en |
| dc.contributor.author | 賴湶敬 | zh_TW |
| dc.date.accessioned | 2021-06-16T05:25:16Z | - |
| dc.date.available | 2014-10-09 | |
| dc.date.copyright | 2014-10-09 | |
| dc.date.issued | 2014 | |
| dc.date.submitted | 2014-08-14 | |
| dc.identifier.citation | Adams, B.W., Bradberry, C.W., and Moghaddam, B. (2002). NMDA antagonist effects on striatal dopamine release: Microdialysis studies in awake monkeys. Synapse 43, 12–18.
Allison, L.A., Mayer, G.S., and Shoup, R.E. (1984). The o-phthalaldehyde derivatives of amines for high-speed liquid chromatography/electrochemistry. Anal. Chem. 56, 1089–1096. Del Arco, A., Castaneda, T.R., and Mora, F. (1998). Amphetamine releases GABA in striatum of the freely moving rat: involvement of calcium and high affinity transporter mechanisms. Neuropharmacology 37, 199–205. Del Arco, A., Gonzalez-Mora, J.L., Armas, V.R., and Mora, F. (1999). Amphetamine increases the extracellular concentration of glutamate in striatum of the awake rat: involvement of high affinity transporter mechanisms. Neuropharmacology 38, 943–954. Bacopoulos, N., Redmond, D., and Roth, R. (1979). Serotonin and dopamine metabolites in brain regions and cerebrospinal fluid of a primate species: effects of ketamine and fluphenazine. J. Neurochem. 32, 1215–1218. Barnett, J.V., and Kuczenski, R. (1986). Desensitization of rat striatal dopamine-stimulated adenylate cyclase after acute amphetamine administration. J. Pharmacol. Exp. Ther. 237, 820–825. Bastian, A.J. (1997). Mechanisms of ataxia. Phys. Ther. 77, 672–675. Becker, A., Peters, B., Schroeder, H., Mann, T., Huether, G., and Grecksch, G. (2003). Ketamine-induced changes in rat behaviour: A possible animal model of schizophrenia. Prog. Neuropsychopharmacol. Biol. Psychiatry 27, 687–700. Behrens, M.M., Ali, S.S., Dao, D.N., Lucero, J., Shekhtman, G., Quick, K.L., and Dugan, L.L. (2007). Ketamine-Induced Loss of Phenotype of Fast-Spiking Interneurons Is Mediated by NADPH-Oxidase. Science 318, 1645–1647. Berman, R.M., Cappiello, A., Anand, A., Oren, D.A., Heninger, G.R., Charney, D.S., and Krystal, J.H. (2000). Antidepressant effects of ketamine in depressed patients. Biol. Psychiatry 47, 351–354. Borison, R.L., Havdala, H.S., and Diamond, B.I. (1977). Chronic phenylethylamine stereotypy in rats: A new animal model for schizophrenia? Life Sci. 21, 117–122. Brown, E.N., Purdon, P.L., and Van Dort, C.J. (2011). General anesthesia and altered states of arousal: a systems neuroscience analysis. Annu. Rev. Neurosci. 34, 601. Butcher, S.P., Fairbrother, I.S., Kelly, J.S., and Arbuthnott, G.W. (1988). Amphetamine-induced dopamine release in the rat striatum: an in vivo microdialysis study. J. Neurochem. 50, 346–355. Callaghan, R.C., Cunningham, J.K., Sykes, J., and Kish, S.J. (2012). Increased risk of Parkinson’s disease in individuals hospitalized with conditions related to the use of methamphetamine or other amphetamine-type drugs. Drug Alcohol Depend. 120, 35–40. Carter, C., and Pycock, C. (1979). The effects of 5, 7-dihydroxytryptamine lesions of extrapyramidal and mesolimbic sites on spontaneous motor behaviour, and amphetamine-induced stereotypy. Naunyn. Schmiedebergs Arch. Pharmacol. 308, 51–54. Champney, T.H., Hanneman, W.H., and Nichols, M.A. (1992). gamma-Aminobutyric acid, catecholamine and indoleamine determinations from the same brain region by high-performance liquid chromatography with electrochemical detection. J. Chromatogr. 579, 334–339. Cowan, R.L., Wilson, C.J., Emson, P.C., and Heizmann, C.W. (1990). Parvalbumin-containing gabaergic interneurons in the rat neostriatum. J. Comp. Neurol. 302, 197–205. Creese, I., and Iversen, S.D. (1974). The role of forebrain dopamine systems in amphetamine induced stereotyped behavior in the rat. Psychopharmacologia 39, 345–357. David Sturgeon, R., Fessler, R.G., and Meltzer, H.Y. (1979). Behavioral rating scales for assessing phencyclidine-induced locomotor activity, stereotypes behavior and ataxia in rats. Eur. J. Pharmacol. 59, 169–179. Dillon, P., Copeland, J., and Jansen, K. (2003). Patterns of use and harms associated with non-medical ketamine use. Drug Alcohol Depend. 69, 23–28. Dittmar, M.S., Fehm, N.P., Vatankhah, B., and Horn, M. (2004). Ketamine/xylazine anesthesia for radiologic imaging of neurologically impaired rats: dose response, respiratory depression, and management of complications. Comp. Med. 54, 652–655. Drevets, W.C., Gautier, C., Price, J.C., Kupfer, D.J., Kinahan, P.E., Grace, A.A., Price, J.L., and Mathis, C.A. (2001). Amphetamine-induced dopamine release in human ventral striatum correlates with euphoria. Biol. Psychiatry 49, 81–96. Floresco, S.B., West, A.R., Ash, B., Moore, H., and Grace, A.A. (2003). Afferent modulation of dopamine neuron firing differentially regulates tonic and phasic dopamine transmission. Nat. Neurosci. 6, 968–973. Di Forti, M., Lappin, J.M., and Murray, R.M. (2007). Risk factors for schizophrenia—all roads lead to dopamine. Eur. Neuropsychopharmacol. 17, S101–S107. Glausier, J.R., Khan, Z.U., and Muly, E.C. (2009). Dopamine D1 and D5 Receptors Are Localized to Discrete Populations of Interneurons in Primate Prefrontal Cortex. Cereb. Cortex 19, 1820–1834. Grace, A. (1991). Phasic versus tonic dopamine release and the modulation of dopamine system responsivity: a hypothesis for the etiology of schizophrenia. Neuroscience 41, 1–24. Grace, A.A., Floresco, S.B., Goto, Y., and Lodge, D.J. (2007). Regulation of firing of dopaminergic neurons and control of goal-directed behaviors. Trends Neurosci. 30, 220–227. Hayase, T., Yamamoto, Y., and Yamamoto, K. (2006). Behavioral effects of ketamine and toxic interactions with psychostimulants. BMC Neurosci. 7, 25. Hayashi, H., Dikkes, P., and Soriano, S.G. (2002). Repeated administration of ketamine may lead to neuronal degeneration in the developing rat brain. Pediatr. Anesth. 12, 770–774. Hitri, A., Hurd, Y.L., Wyatt, R.J., and Deutsch, S.I. (1994). Molecular, functional and biochemical characteristics of the dopamine transporter: regional differences and clinical relevance. Clin. Neuropharmacol. 17, 1–22. Homayoun, H., and Moghaddam, B. (2007). NMDA Receptor Hypofunction Produces Opposite Effects on Prefrontal Cortex Interneurons and Pyramidal Neurons. J. Neurosci. 27, 11496–11500. Hunt, M.J., Raynaud, B., and Garcia, R. (2006). Ketamine Dose-Dependently Induces High-Frequency Oscillations in the Nucleus Accumbens in Freely Moving Rats. Biol. Psychiatry 60, 1206–1214. Ikonomidou, C., Bosch, F., Miksa, M., Bittigau, P., Vockler, J., Dikranian, K., Tenkova, T.I., Stefovska, V., Turski, L., and Olney, J.W. (1999). Blockade of NMDA receptors and apoptotic neurodegeneration in the developing brain. Science 283, 70–74. Imre, G., Fokkema, D.S., and Ter Horst, G.J. (2006). Subchronic administration of LY354740 does not modify ketamine-evoked behavior and neuronal activity in rats. Eur. J. Pharmacol. 544, 77–81. Irifune, M., Fukuda, T., Nomoto, M., Sato, T., Kamata, Y., Nishikawa, T., Mietani, W., Yokoyama, K., Sugiyama, K., and Kawahara, M. (1997). Effects of ketamine on dopamine metabolism during anesthesia in discrete brain regions in mice: comparison with the effects during the recovery and subanesthetic phases. Brain Res. 763, 281–284. Jansen, K.L. (2000). A review of the nonmedical use of ketamine: use, users and consequences. J. Psychoactive Drugs 32, 419–433. Jerram, A.H., Smith, P.F., and Darlington, C.L. (1996). The effects of ♁-SKF10047 and ketamine hydrochloride on stereotyped behaviour, locomotor activity and ataxia in guinea pig. Eur. J. Pharmacol. 307, 269–273. Jones, S.R., Gainetdinov, R.R., Wightman, R.M., and Caron, M.G. (1998). Mechanisms of amphetamine action revealed in mice lacking the dopamine transporter. J. Neurosci. 18, 1979–1986. Kahlig, K.M., Binda, F., Khoshbouei, H., Blakely, R.D., McMahon, D.G., Javitch, J.A., and Galli, A. (2005). Amphetamine induces dopamine efflux through a dopamine transporter channel. Proc. Natl. Acad. Sci. U. S. A. 102, 3495–3500. Kalsi, S.S., Wood, D.M., and Dargan, P.I. (2011). The epidemiology and patterns of acute and chronic toxicity associated with recreational ketamine use. Emerg. Health Threats J. 4. Kawaguchi, Y., Wilson, C.J., Augood, S.J., and Emson, P.C. (1995). Striatal interneurones: chemical, physiological and morphological characterization. Trends Neurosci. 18, 527–535. Ke, J.-J., Chen, H.-I., Jen, C.J., Kuo, Y.-M., Cherng, C.G., Tsai, Y.-P.N., Ho, M.-C., Tsai, C.-W., and Yu, L. (2008). Mutual enhancement of central neurotoxicity induced by ketamine followed by methamphetamine. Toxicol. Appl. Pharmacol. 227, 239–247. Kegeles, L.S., Abi-Dargham, A., Zea-Ponce, Y., Rodenhiser-Hill, J., Mann, J.J., Van Heertum, R.L., Cooper, T.B., Carlsson, A., and Laruelle, M. (2000). PRIORITY COMMUNICATIONS. Biol Psychiatry 48, 627–640. Kemppainen, S., and Pitkanen, A. (2000). Distribution of parvalbumin, calretinin, and calbindin-D(28k) immunoreactivity in the rat amygdaloid complex and colocalization with gamma-aminobutyric acid. J. Comp. Neurol. 426, 441–467. Kessal, K., Chessel, A., Spennato, G., and Garcia, R. (2005). Ketamine and amphetamine both enhance synaptic transmission in the amygdala-nucleus accumbens pathway but with different time-courses. Synapse 57, 61–65. Krystal, J.H., Perry, E.B., Gueorguieva, R., Belger, A., Madonick, S.H., Abi-Dargham, A., Cooper, T.B., MacDougall, L., Abi-Saab, W., and D’Souza, D.C. (2005). Comparative and interactive human psychopharmacologic effects of ketamine and amphetamine: implications for glutamatergic and dopaminergic model psychoses and cognitive function. Arch. Gen. Psychiatry 62, 985–995. Kubota, T., Hirota, K., Yoshida, H., Takahashi, S., Ohkawa, H., Anzawa, N., Kuhshikata, T., and Matsuki, A. (1999). Inhibitory effect of clonidine on ketamine-induced norepinephrine release from the medial prefrontal cortex in rats. Br. J. Anaesth. 83, 945–947. Kubota, Y., Inagaki, S., Kito, S., and Wu, J.-Y. (1987a). Dopaminergic axons directly make synapses with GABAergic neurons in the rat neostriatum. Brain Res. 406, 147–156. Kubota, Y., Inagaki, S., Shimada, S., Kito, S., Eckenstein, F., and Tohyama, M. (1987b). Neostriatal cholinergic neurons receive direct synaptic inputs from dopaminergic axons. Brain Res. 413, 179–184. Kuczenski, R., and Segal, D.S. (1975). Differential effects of D-and L-amphetamine and methylphenidate on rat striatal dopamine biosynthesis. Eur. J. Pharmacol. 30, 244–251. Kuczenski, R., Segal, D.S., and Todd, P.K. (1997). Behavioral sensitization and extracellular dopamine responses to amphetamine after various treatments. Psychopharmacology (Berl.) 134, 221–229. Lai, C.-C., Lee, L.-J., and Yin, H.-S. (2013). Combinational effects of ketamine and amphetamine on behaviors and neurotransmitter systems of mice. Neurotoxicology 37, 136–143. Lankenau, S.E., and Clatts, M.C. (2005). Patterns of polydrug use among ketamine injectors in New York City. Subst. Use Misuse 40, 1381–1397. Liao, Y., Tang, J., Fornito, A., Liu, T., Chen, X., Chen, H., Xiang, X., Wang, X., and Hao, W. (2012). Alterations in regional homogeneity of resting-state brain activity in ketamine addicts. Neurosci. Lett. 522, 36–40. Lindefors, N., Barati, S., and O’Connor, W.T. (1997). Differential effects of single and repeated ketamine administration on dopamine, serotonin and GABA transmission in rat medial prefrontal cortex. Brain Res. 759, 205–212. Lisman, J.E., Coyle, J.T., Green, R.W., Javitt, D.C., Benes, F.M., Heckers, S., and Grace, A.A. (2008). Circuit-based framework for understanding neurotransmitter and risk gene interactions in schizophrenia. Trends Neurosci. 31, 234–242. Liu, C., Li, J., Tsay, W., and Hsu, J. (2005). Drug use and profile of individuals arrested on drug-related charges in Taiwan. J. Food Drug Anal. 13, 101. Liu, C.H., Ren, J.Q., Yang, J., Liu, C., Mandeville, J.B., Rosen, B.R., Bhide, P.G., Yanagawa, Y., and Liu, P.K. (2009). DNA-based MRI probes for specific detection of chronic exposure to amphetamine in living brains. J. Neurosci. 29, 10663–10670. Lorrain, D.., Baccei, C.., Bristow, L.., Anderson, J.., and Varney, M.. (2003). Effects of ketamine and n-methyl-d-aspartate on glutamate and dopamine release in the rat prefrontal cortex: modulation by a group II selective metabotropic glutamate receptor agonist LY379268. Neuroscience 117, 697–706. Martin, L.L., and Smith, D.J. (1982). Ketamine inhibits serotonin synthesis and metabolism in vivo. Neuropharmacology 21, 119–125. Martin, L.L., Bouchal, R.L., and Smith, D.J. (1982). Ketamine inhibits serotonin uptake in vivo. Neuropharmacology 21, 113–118. Martinez, D., Narendran, R., Foltin, R., Slifstein, M., Hwang, D.-R., Broft, A., Huang, Y., Cooper, T., Fischman, M., Kleber, H., et al. (2007). Amphetamine-induced dopamine release: markedly blunted in cocaine dependence and predictive of the choice to self-administer cocaine. Am. J. Psychiatry 164, 622–629. Masuzawa, M., Nakao, S., Miyamoto, E., Yamada, M., Murao, K., Nishi, K., and Shingu, K. (2003). Pentobarbital inhibits ketamine-induced dopamine release in the rat nucleus accumbens: a microdialysis study. Anesth. Analg. 96, 148–152. Meliska, C.J., and Trevor, A.J. (1978). Differential effects of ketamine on schedule-controlled responding and motility. Pharmacol. Biochem. Behav. 8, 679–683. Middleton, F.A., and Strick, P.L. (2000). Basal Ganglia Output and Cognition: Evidence from Anatomical, Behavioral, and Clinical Studies. Brain Cogn. 42, 183–200. Middleton, J.W., Kiritani, T., Pedersen, C., Turner, J.G., Shepherd, G.M., and Tzounopoulos, T. (2011). Mice with behavioral evidence of tinnitus exhibit dorsal cochlear nucleus hyperactivity because of decreased GABAergic inhibition. Proc. Natl. Acad. Sci. 108, 7601–7606. Miele, M., Mura, M.A., Enrico, P., Esposito, G., Serra, P.A., Migheli, R., Zangani, D., Miele, E., and Desole, M.S. (2000). On the mechanism of d-amphetamine-induced changes in glutamate, ascorbic acid and uric acid release in the striatum of freely moving rats. Br. J. Pharmacol. 129, 582–588. Miettinen, M., Pitkanen, A., and Miettinen, R. (1997). Distribution of calretinin-immunoreactivity in the rat entorhinal cortex: Coexistence with GABA. J. Comp. Neurol. 378, 363–378. Moghaddam, B., Adams, B., Verma, A., and Daly, D. (1997). Activation of glutamatergic neurotransmission by ketamine: a novel step in the pathway from NMDA receptor blockade to dopaminergic and cognitive disruptions associated with the prefrontal cortex. J. Neurosci. 17, 2921–2927. Le Moine, C., Normand, E., and Bloch, B. (1991). Phenotypical characterization of the rat striatal neurons expressing the D1 dopamine receptor gene. Proc. Natl. Acad. Sci. 88, 4205–4209. Morgan, C.J., and Curran, H.V. (2012). Ketamine use: a review. Addiction 107, 27–38. Nicolas, M.J., Lopez-Azcarate, J., Valencia, M., Alegre, M., Perez-Alcazar, M., Iriarte, J., and Artieda, J. (2011). Ketamine-induced oscillations in the motor circuit of the rat basal ganglia. PloS One 6, e21814. Paule, M., Li, M., Allen, R., Liu, F., Zou, X., Hotchkiss, C., Hanig, J., Patterson, T., Slikker Jr, W., and Wang, C. (2011). Ketamine anesthesia during the first week of life can cause long-lasting cognitive deficits in rhesus monkeys. Neurotoxicol. Teratol. 33, 220–230. Peleg-Raibstein, D., Knuesel, I., and Feldon, J. (2008). Amphetamine sensitization in rats as an animal model of schizophrenia. Behav. Brain Res. 191, 190–201. Pifl, C., Drobny, H., Reither, H., Hornykiewicz, O., and Singer, E.A. (1995). Mechanism of the dopamine-releasing actions of amphetamine and cocaine: plasmalemmal dopamine transporter versus vesicular monoamine transporter. Mol. Pharmacol. 47, 368–373. Post, R.M., and Rose, H. (1976). Increasing effects of repetitive cocaine administration in the rat. Reid, M.S., Hsu Jr, K., and Berger, S.P. (1997). Cocaine and amphetamine preferentially stimulate glutamate release in the limbic system: studies on the involvement of dopamine. Synapse 27, 95–105. Reynolds, G.P., Abdul-Monim, Z., Neill, J.C., and Zhang, Z.-J. (2004). Calcium binding protein markers of GABA deficits in schizophrenia—post mortem studies and animal models. Neurotox. Res. 6, 57–61. Robinson, T.E., and Berridge, K.C. (1993). The neural basis of drug craving: an incentive-sensitization theory of addiction. Brain Res. Rev. 18, 247–291. Rowley, H.L., Martin, K.F., and Marsden, C.A. (1995). Determination of in vivo amino acid neurotransmitters by high-performance liquid chromatography with< i> o</i>-phthalaldehyde-sulphite derivatisation. J. Neurosci. Methods 57, 93–99. Saunders, C., Ferrer, J.V., Shi, L., Chen, J., Merrill, G., Lamb, M.E., Leeb-Lundberg, L.F., Carvelli, L., Javitch, J.A., and Galli, A. (2000). Amphetamine-induced loss of human dopamine transporter activity: an internalization-dependent and cocaine-sensitive mechanism. Proc. Natl. Acad. Sci. 97, 6850–6855. Segal, D.S., and Mandell, A.J. (1974). Long-term administration of d-amphetamine: progressive augmentation of motor activity and stereotypy. Pharmacol. Biochem. Behav. 2, 249–255. Seiden, L.S., Sabol, K.E., and Ricaurte, G.A. (1993). Amphetamine: effects on catecholamine systems and behavior. Annu. Rev. Pharmacol. Toxicol. 33, 639–676. Slikker, W., Zou, X., Hotchkiss, C.E., Divine, R.L., Sadovova, N., Twaddle, N.C., Doerge, D.R., Scallet, A.C., Patterson, T.A., Hanig, J.P., et al. (2007). Ketamine-induced neuronal cell death in the perinatal rhesus monkey. Toxicol. Sci. 98, 145–158. Soghomonian, J.-J., and Chesselet, M.-F. (1992). Effects of nigrostriatal lesions on the levels of messenger RNAs encoding two isoforms of glutamate decarboxylase in the globus pallidus and entopeduncular nucleus of the rat. Synapse 11, 124–133. Tso, M. (2004). Stereoselective effects of ketamine on dopamine, serotonin and noradrenaline release and uptake in rat brain slices. Neurochem. Int. 44, 1–7. Uchihashi, Y., Kuribara, H., and Tadokoro, S. (1992). Assessment of the ambulation-increasing effect of ketamine by coadministration with central-acting drugs in mice. Jpn. J. Pharmacol. 60, 25–31. Vanderwende, C., Spoerlein, M.T., and Lapollo, J. (1982). Cocaine potentiates ketamine-induced loss of the righting reflex and sleeping time in mice. Role of catecholamines. J. Pharmacol. Exp. Ther. 222, 122–125. White, F.J., and Kalivas, P.W. (1998). Neuroadaptations involved in amphetamine and cocaine addiction. Drug Alcohol Depend. 51, 141–153. White, J.M., and Ryan, C.F. (1996). Pharmacological properties of ketamine. Drug Alcohol Rev. 15, 145–155. White, P.F., Way, W.L., and Trevor, A.J. (1982). Ketamine--its pharmacology and therapeutic uses. Anesthesiology 56, 119–136. Whitton, P.S. (1997). Glutamatergic control over brain dopamine release in vivo and in vitro. Neurosci. Biobehav. Rev. 21, 481–488. Wilson, C., Kercher, M., Quinn, B., Murphy, A., Fiegel, C., and McLaurin, A. (2007). Effects of age and sex on ketamine-induced hyperactivity in rats. Physiol. Behav. 91, 202–207. Wong, A.H.C., and Van Tol, H.H.M. (2003). Schizophrenia: from phenomenology to neurobiology. Neurosci. Biobehav. Rev. 27, 269–306. Wong, D.H., and Jenkins, L.C. (1974). An experimental study of the mechanism of action of ketamine on the central nervous system. Can. Anaesth. Soc. J. 21, 57–67. Wright, M. (1982). Pharmacologic effects of ketamine and its use in veterinary medicine [Anesthesia]. J. Am. Vet. Med. Assoc. Xu, D., Mo, Z., Yung, K., Yang, Y., and Leung, A. (2008). Individual and combined effects of methamphetamine and ketamine on conditioned place preference and NR1 receptor phosphorylation in rats. Neurosignals 15, 322–331. Yadid, G., Pacak, K., Kopin, I.J., and Goldstein, D.S. (1994). Endogenous serotonin stimulates striatal dopamine release in conscious rats. J. Pharmacol. Exp. Ther. 270, 1158–1165. Yang, C.R., Seamans, J.K., and Gorelova, N. (1999). Developing a neuronal model for the pathophysiology of schizophrenia based on the nature of electrophysiological actions of dopamine in the prefrontal cortex. Neuropsychopharmacology 21, 161–194. Yin, H.-S., and Tan, H.-W. (2007). Effects of amphetamine on serotoninergic and GABAergic expression of developing brain. Neurotoxicol. Teratol. 29, 264–272. Yin, H.-S., Chen, C.-T., and Lin, T.-Y. (2004). Age- and region-dependent alterations in the GABAergic innervation in the brain of rats treated with amphetamine. Int. J. Neuropsychopharmacol. 7, 35–48. Yin, H.-S., Chen, K., Kalpana, S., and Shih, J.C. (2006). Differential effects of chronic amphetamine and baclofen administration on cAMP levels and phosphorylation of CREB in distinct brain regions of wild type and monoamine oxidase B-deficient mice. Synapse 60, 573–584. Yin, H.-S., Cheng, P.-R., and Chen, C.-S. (2009). Differential alterations in the relations among GABAergic, catecholaminergic and calcium binding protein expression in the olfactory bulb of amphetamine-administered mouse. NeuroToxicology 30, 103–113. Yin, H.-S., Lai, C.-C., Tien, T.-W., Han, S.-K., and Pu, X.-L. (2010). Differential changes in cerebellar transmitter content and expression of calcium binding proteins and transcription factors in mouse administered with amphetamine. Neurochem. Int. 57, 288–296. Yin, H.-S., Tien, T.-W., Li, L., Yang, Y.-H., and Lai, C.-C. (2012). Amphetamine differentially modifies the expression of monoaminergic and GABAergic synaptic boutons and processes in lateral habenula, dorsal and ventral hippocampal formation. Neurotoxicology 33, 235–245. Zetterstrom, T., Sharp, T., and Ungerstedt, U. (1986). Further evaluation of the mechanism by which amphetamine reduces striatal dopamine metabolism: a brain dialysis study. Eur. J. Pharmacol. 132, 1–9. Zhang, Y., Behrens, M.M., and Lisman, J.E. (2008). Prolonged Exposure to NMDAR Antagonist Suppresses Inhibitory Synaptic Transmission in Prefrontal Cortex. J. Neurophysiol. 100, 959–965. | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/56365 | - |
| dc.description.abstract | 吸毒者常合併攝入氯胺酮(ketamine; Ket)與安非他命(amphetamine; Amph)並造成嚴重的行為異常。大量的研究表明,多重藥物使用引起行為與神經化學的變化,但是這兩種藥物交互的影響仍然未明。在本研究中,我們對年輕公鼠作腹腔注射生理食鹽水(saline)、安非他命(Amph, 5 mg/kg)、低劑量氯胺酮(low Ket; LK, 10 mg/kg)、 高劑量氯胺酮(high Ket; HK, 50 mg/kg)、或是安非他命加上低劑量或者高劑量氯胺酮(ALK 或 AHK)。注射分成單次注射或者四天七劑重複注射,以探討氯胺酮與安非他命引起的早期變化。藥物施打之後,我們在開放式領域中檢測包括運動、刻板行為、與共濟失調等動物行為。相較於生理食鹽水組的小鼠,單獨注射 Amph、LK、HK會增加運動、刻板行為、與共濟失調等行為的活性。在合併處理的組別中,LK 與 HK 會增加 Amph引起的運動及刻板行為。值得注意的是,不論單次或重複藥物處理, Amph 會增強 Ket 所誘發的共濟失調。在單次 Amph、ALK、AHK處理時,小鼠較強的運動活性與紋狀體中多巴胺含量較高有關。ALK與AHK小鼠較長時間的行為活性與較高的運動行為,可能與運動皮質中多巴胺增加的時間延長有關;在這些小鼠中,較嚴重的共濟失調,可能與體感覺皮質中較高的多巴胺濃度有關。在重複處理時,最後一次注射完畢後四小時,行為的活性已經消退,但運動相關皮質中多巴胺的含量仍有明顯變化,意味著多巴胺系統的調節受到藥物重複處理的影響。除此之外,不論單次或重複藥物處理,GAD67陽性的點狀結構小點在紋狀體與運動相關皮質的表現,仍高於生理食鹽水的控制組,推測γ-氨基丁酸系統的神經特性也有適應性的改變。我們的結果首次表明了安非他命與氯胺酮,在急性或者重複處理時,行為與神經化學方面的交互作用,並顯示了γ-氨基丁酸與多巴胺系統的神經適應性變化。 | zh_TW |
| dc.description.abstract | The combined ingestion of ketamine (Ket) and amphetamine (Amph) by drug-users has been rampant and produced more severe behavioral abnormality than each individual ingestion. Numerous studies illustrate the behavioral and neurochemical changes of polydrug administration; however, the interactive consequences of the two drugs are still unclear. In this study, young adult mice were intraperitoneally injected with saline, Amph (5 mg/kg), low Ket (LK, 10 mg/kg), high Ket (HK, 50 mg/kg), or Amph plus LK or HK (ALK or AHK). Single treatment or 7 repetitive treatments within 4 days were conducted. Animal behaviors, including locomotion, stereotypy and ataxia, were examined in a novel open field. Compared with saline, Amph, LK or HK treatment alone increased the levels of motor activities such as locomotion, stereotypy or ataxia of mice. At combined treatments, LK and HK differentially exacerbated Amph-induced locomotion and stereotypy. Notably, Amph-mediated potentiation in Ket-triggered ataxia were manifested after single or repeated drug treatments. After single treatment, the higher striatal dopamine levels of A, ALK and AHK groups correlated with their greater motor activities. The prolonged increase of dopamine in the motor cortex of ALK and AHK mice may associate with the longer duration of behavioral hyperactivity and greater peak score of locomotion; the greater dopamine level in the somatosensory cortex probably contributes to the more severe ataxia. For repetitive treatments, four hours after the final treatment, while the behavioral hyperactivities were ceased, considerable changes were still evident in the motor-related cortices, suggesting modulation to the DAergic system. Furthermore, a significant increase in the number of GAD67-positive puncta in the striatum and motor-related cortices were higher than respective saline controls after both single and repetitive treatments, suggesting a neural adaptive change in the GABAergic system. Our results demonstrate the first time the acute and receptive interplay between Amph and Ket in both behavioral and neurochemical aspects, and show neural adaptive changes in the GABAergic and DAergic systems. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-16T05:25:16Z (GMT). No. of bitstreams: 1 ntu-103-D92446001-1.pdf: 7397773 bytes, checksum: f9f74a7831c3fd809befa5538a58e910 (MD5) Previous issue date: 2014 | en |
| dc.description.tableofcontents | 中文摘要 .............................................................. 1
Abstract …............................................................ 3 General Introduction ........................................... 5 Part 1: Combinational Effects of Ketamine and Amphetamine on Behaviors and Neurotransmitter Systems of Mice - Abstract ........................................................... 11 - Introduction .................................................... 13 - Materials & Methods ......................................... 16 - Results ............................................................ 24 - Discussion ....................................................... 30 - Conclusion ...................................................... 34 - Figure Legends ................................................ 35 Part 2: Behavioral and neurochemical changes induced by repetitive combined treatments of ketamine and amphetamine in mice - Abstract .......................................................... 57 - Introduction ................................................... 59 - Materials & Methods ........................................ 62 - Results ........................................................... 68 - Discussion ...................................................... 76 - Figure Legends ................................................ 81 General Discussion …........................................ 100 Conclusion and Prospects ................................ 105 Reference ....................................................... 107 | |
| dc.language.iso | en | |
| dc.subject | 藥物濫用 | zh_TW |
| dc.subject | 動物模式 | zh_TW |
| dc.subject | 活動亢進 | zh_TW |
| dc.subject | γ-氨基丁酸系統 | zh_TW |
| dc.subject | 多巴胺系統 | zh_TW |
| dc.subject | dopaminergic system | en |
| dc.subject | animal model | en |
| dc.subject | hyperactivity | en |
| dc.subject | GABAergic system | en |
| dc.subject | drug abuse | en |
| dc.title | 氯胺酮與安非他命合併處理小鼠之皮質與基底核前期變化 | zh_TW |
| dc.title | Early Changes in the Cortices and Basal Ganglia Induced by Combined Treatments of Ketamine and Amphetamine in Mice | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 102-2 | |
| dc.description.degree | 博士 | |
| dc.contributor.coadvisor | 李立仁(Li-Jen Lee) | |
| dc.contributor.oralexamcommittee | 蕭水銀(Shoei-Yn Lin-Shiau),呂俊宏(June-Horng Lue),黃智偉(Andrew Chih-Wei Huang) | |
| dc.subject.keyword | 藥物濫用,動物模式,活動亢進,γ-氨基丁酸系統,多巴胺系統, | zh_TW |
| dc.subject.keyword | drug abuse,animal model,hyperactivity,GABAergic system,dopaminergic system, | en |
| dc.relation.page | 125 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2014-08-15 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 解剖學暨細胞生物學研究所 | zh_TW |
| 顯示於系所單位: | 解剖學暨細胞生物學科所 | |
文件中的檔案:
| 檔案 | 大小 | 格式 | |
|---|---|---|---|
| ntu-103-1.pdf 未授權公開取用 | 7.22 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。
