铜对大鼠海马CAl区神经元A-电流和延迟整流钾电流的影响
|
摘要
铜是一种重要的过渡金属，在中枢神经系统中起着重要的作用。但是，铜代谢的紊乱对中枢神经系统是有害的，尤其是铜浓度过度升高时。中枢神经元中含铜量病理性的升高会引起严重的神经学紊乱，如神经退行性病变和智力障碍，人们推测这与威尔逊病(WD)和阿尔茨海默病(AD)的发病机制有关。近来的研究表明，电压依赖性钾通道的功能异常与学习和记忆的损伤、共济失调、癫痫、神经性耳聋等一些神经性疾病的产生有关，其中电压依赖性瞬间外向钾通道和延迟整流钾通道的功能还与学习和记忆有关。由于WD患者和AD的早期患者的脑部海马均含有高水平的铜，故在本课题中，我们应用全细胞膜片钳技术，在急性分离的大鼠海马CA1区锥体神经元上比较详细地研究生理和病理浓度的Cu~(2+)对电压依赖性瞬间外向钾电流(L_A)和延迟整流钾电流(I_K)的效应。主要研究结果如下：
1．急性铜暴露对大鼠海马CA1区神经元A-型钾电流的影响
胞外1，10，30，100和1000μM Cu~(2+)以剂量依赖性的方式可逆地抑制I_A的幅度，其IC_(50)值为130μM。较高浓度的铜，即100和300μM Cu~(2+)能显著地使I_A的激活曲线向去极化方向移动(V_(1/2):对照，1.0±0.2mV；100μM Cu~(2+)，8.2±1.1mV；300μM Cu~(2+)，18.2±1.1mV)，提示Cu~(2+)抑制I_A的激活。对于稳态失活曲线，100和300μM Cu~(2+)也能显著地使其向去极化方向移动(V_(1/2):对照，-87.7±2.0mV；100μM Cu~(2+)，-82.5±0.5mV；300μM Cu~(2+)，-78.7±1.5mV)，提示在任何一个给定的膜电位处，通道的失活受到Cu~(2+)的抑制。此外，100和300μM Cu~(2+)还能明显促进A-型钾通道的失活，并减缓通道从失活状态的恢复。结果提示：生理和病理浓度的Cu~(2+)可能通过对A-型钾通道的抑制影响大鼠海马CA1区神经元的兴奋性。而这也可能涉及到WD和早期阶段AD的病理过程，并可能与WD病人的智力障碍以及AD患者早期记忆丧失和认知功能下降有关。
2．铜对急性分离的大鼠海马CA1区神经元延迟整流钾电流的抑制
胞外1，10，30，100和1000μM Cu~(2+)以剂量依赖性的方式可逆地抑制I_K的幅度，且高浓度的Cu~(2+)(1000μM)对I_K的抑制也仅仅为64％。其IC_(50)值为100
Copper (Cu~(2+)) is an essential transition metal that plays a critical role in the central nervous system (CNS). However, aberrant copper homeostasis is harmful to CNS and excess copper is extremely toxic in the CNS. Pathologically increased accumulation of copper in central neurons induce severe neurological disorders, such as neurological degeneration, mental retardation, which has been postulated to play a role in the pathogenesis of Wilson's disease (WD) and Alzheimer's disease (AD). Recently, many human neurological disease pathgenesis has been shown to be related to abnormalities of voltage-gated K~+ channel function, such as learning and memory impairing, ataxia, epilepsy and deafness. Recent evidence demonstrated that voltage-dependent transient outward and delayed rectifier K~+ channel function have been implicated in learning and memory. In addition, high concentrations of Cu~(2+) has been measured in the brain for patients with WD or AD. Thus, in this study, we investigated in detail the effects of physiologically and pathologically relevant copper on I_a and I_k by using the whole-cell patch-clamp technique in the acutely dissociated rat hippocampal CA1 pyramid neurons. The main results were summarized as following:
1. Effects of copper on A-type potassium currents (I_A) in acutely dissociated rat
hippocampal CA1 neurons
Extracellular application of various concentrations of Cu~(2+)(1-1000 μM) reversibly reduced the amplitude of I_a in a dose-dependent manner with an IC_(50) value of 130 μM. 100 and 300 μM Cu~(2+)significantly shifted the V_(1/2) of steady-state activation curve to the depolarizing direction by 7.2 and 17.2 mV, respectively, indicating that Cu~(2+) decreased the activation of I_a. For state-inactivation curves, 100 and 300 μM Cu~(2+) markedly shifted the V_(1/2) to the depolarizing direction by 5.2 and 9.0 mV, respectively, indicating that channels were less likely to be inactivated at higher concentrations of Cu~(2+) at any given potential. In addition, higher concentrations Cu~(2+) markedly increased the decay at a prepulse potential of -110 mV and significantly slowed the recovery of I_k from inactivation. These results suggest it is possible for
1．急性铜暴露对大鼠海马CA1区神经元A-型钾电流的影响
胞外1，10，30，100和1000μM Cu~(2+)以剂量依赖性的方式可逆地抑制I_A的幅度，其IC_(50)值为130μM。较高浓度的铜，即100和300μM Cu~(2+)能显著地使I_A的激活曲线向去极化方向移动(V_(1/2):对照，1.0±0.2mV；100μM Cu~(2+)，8.2±1.1mV；300μM Cu~(2+)，18.2±1.1mV)，提示Cu~(2+)抑制I_A的激活。对于稳态失活曲线，100和300μM Cu~(2+)也能显著地使其向去极化方向移动(V_(1/2):对照，-87.7±2.0mV；100μM Cu~(2+)，-82.5±0.5mV；300μM Cu~(2+)，-78.7±1.5mV)，提示在任何一个给定的膜电位处，通道的失活受到Cu~(2+)的抑制。此外，100和300μM Cu~(2+)还能明显促进A-型钾通道的失活，并减缓通道从失活状态的恢复。结果提示：生理和病理浓度的Cu~(2+)可能通过对A-型钾通道的抑制影响大鼠海马CA1区神经元的兴奋性。而这也可能涉及到WD和早期阶段AD的病理过程，并可能与WD病人的智力障碍以及AD患者早期记忆丧失和认知功能下降有关。
2．铜对急性分离的大鼠海马CA1区神经元延迟整流钾电流的抑制
胞外1，10，30，100和1000μM Cu~(2+)以剂量依赖性的方式可逆地抑制I_K的幅度，且高浓度的Cu~(2+)(1000μM)对I_K的抑制也仅仅为64％。其IC_(50)值为100
Copper (Cu~(2+)) is an essential transition metal that plays a critical role in the central nervous system (CNS). However, aberrant copper homeostasis is harmful to CNS and excess copper is extremely toxic in the CNS. Pathologically increased accumulation of copper in central neurons induce severe neurological disorders, such as neurological degeneration, mental retardation, which has been postulated to play a role in the pathogenesis of Wilson's disease (WD) and Alzheimer's disease (AD). Recently, many human neurological disease pathgenesis has been shown to be related to abnormalities of voltage-gated K~+ channel function, such as learning and memory impairing, ataxia, epilepsy and deafness. Recent evidence demonstrated that voltage-dependent transient outward and delayed rectifier K~+ channel function have been implicated in learning and memory. In addition, high concentrations of Cu~(2+) has been measured in the brain for patients with WD or AD. Thus, in this study, we investigated in detail the effects of physiologically and pathologically relevant copper on I_a and I_k by using the whole-cell patch-clamp technique in the acutely dissociated rat hippocampal CA1 pyramid neurons. The main results were summarized as following:
1. Effects of copper on A-type potassium currents (I_A) in acutely dissociated rat
hippocampal CA1 neurons
Extracellular application of various concentrations of Cu~(2+)(1-1000 μM) reversibly reduced the amplitude of I_a in a dose-dependent manner with an IC_(50) value of 130 μM. 100 and 300 μM Cu~(2+)significantly shifted the V_(1/2) of steady-state activation curve to the depolarizing direction by 7.2 and 17.2 mV, respectively, indicating that Cu~(2+) decreased the activation of I_a. For state-inactivation curves, 100 and 300 μM Cu~(2+) markedly shifted the V_(1/2) to the depolarizing direction by 5.2 and 9.0 mV, respectively, indicating that channels were less likely to be inactivated at higher concentrations of Cu~(2+) at any given potential. In addition, higher concentrations Cu~(2+) markedly increased the decay at a prepulse potential of -110 mV and significantly slowed the recovery of I_k from inactivation. These results suggest it is possible for
引文
[1] Adey WR, Dunlop CW, Hendrix CE. Hippocampal slow waves. Distribution and phase relationships in the course of approach learning. Arch Neurol 1960(3): 74-90.
[2] Barinaga M. Is nitric oxide the "retrograde messenger"? Science 1991(254): 1296-1297.
[3] Bear MF, Dudek SM and Gold JT. Homosynaptic long-term depression in CA1 of rat hippocampus in vitro. Soc. Neurosci Abstr 1992(17): 533.
[4] Berger TW. Long-term potentiation of hippocampal synaptic transmission affects rate of behavioral leaming. Science 1984(224): 627-630.
[5] Bliss TV. Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path. J Physiol 1973(232): 331-356.
[6] Bliss TV and Collibgridge GL. A synaptic model of memory: long-term potentiation in the hippocampus. Nature, 1993, 361:31-39.
[7] Giese KP, Storm JF, Reuter D, Fedorov NB, Shao LR, Leicher T, Pongs O and Silva AJ. Reduced K~+ channel inactivation, spike broadening, and after hyperpolarization in Kvβ 1.1-deficient mice with impaired learning. Learn Mere 1998(5): 257-273.
[8] Giese KP, Peters M, Vemon J. Modulation of excitability as a learning and memory mechanism: A molecular genetic perspective. Physiol Behav 2001(73): 803-810.
[9] 韩太真、吴馥梅主编，学习与记忆的神经生物学。北京医科大学、中国协和大学联合出版社 1998。
[10] Hebb DO. The organization of behavior. Wiley, New York, 1949.
[11] Huang SC, Carson RE, Hoffman EJ, Kuhl DE, Phelps ME. An investigation of a doubletracer technique for positron computerized tomography. J Nucl Med 1982(23): 816-822.
[12] Huerta PT, Lisman JE. Synaptic plasticity during the cholinergic theta- frequency oscillation in vitro. Hippocampus 1996(6): 58-61.
[13] Ito M. Long-term depression. Ann. Rev. Neurosci., 1989, 12: 85-102.
[14] 蒋文，肖鹏，徐世彤。齿状回习得性LTP的形成与θ节律的变化。生理学报 1995(12)：67．
[15] Kirkwood A, Rioult M and Bear MF. Experience-dependent modification of synaptic plastiity in visual cortex. Nature 1996(381): 526-528.
[16] Linden DJ and Connor JA. Long-term depression. Ann Rev Neurosci 1995(18): 319- 357.
[17] Lomon T. Frequence potentiation of excitatory synaptic activity in the dentate area of the hippocampal formation. Acta physiol Scond 1996(68) ( supp 1): 277.
[18] MacVinish LJ, Guo Y, Dixon AK, Murrell-Lagnado, RD, Cuthbert, AW. XE991 reveals differences in K~+ channels regulating chloride secretion in murine airway and colonic epithelium. Mol Pharmacol 2001(60): 753-760.
[19] Orr G, Rao G, Houston FP, McNaughton BL, Barnes CA. Hippocampal synaptic plasticity is modulated by theta rhythm in the fascia dentata of adult and aged freely behaving rats. Hippocampus 2001(11): 647-654.
[20] Racine RJ, Milgram NW and Hafner S. Long-term potentiation phenomena in the rat limbic forebrain. Brain Res 1983(260): 217-232.
[21] Ranck JB Jr. Studies on single neurons in dorsal hippocampal formation and septum in unrestrained rats. I. Behavioral correlates and firing repertoires. Exp Neurol 1973(41): 461-531.
[22] Sato N, Yamaguchi Y. Memory encoding by theta phase precession in the hippocampal net work. Neural Comput 2003(15): 2379-2397.
[23] Scoville WB and Milner B. Loss of recent memory after bilateral hippocampal lesions. J Neurol Neurosurg Psych 1957(20): 11-21.
[24] Watabe AM, O'Dell TJ. Age-related changes in theta frequency stimulation-induced long-term potentiation. Neurobiol Aging 2003(24): 267-272.
[25] Watkins JC and Evans RH. Excitatory amino acid transmitters. Ann Rev Pharmacol Toxicol 1981(21): 165-204.
[26] 吴馥梅，萧信生。学习记忆及其脑内突触机制。自然杂志199l(14)：746-751．
[1] Chabbertet C, Chambard JM, Sans A, Desmadryl G. Three types of depolarization-activated potassium currents in acutely isolated mouse vestibular neurons. J Neurophysiol 2001(85): 1017-1026.
[2] Coetzee WA, Amarillo Y, Chiu J, Chow A, Lau D, McCormack T, Moreno H, Nadal MS, Ozaita A, Pountney D, Saganich M, Vega-Saenz de Miera E, Rudy B. Molecular diversity of K~+ channels. Ann NY Acad Sci 1993(868): 233-285.
[3] Erisir A., Lau D., Rudy B., Leonard C.S. Function of specific K~+ channels in sustained high frequency firing of fast-spiking neocortical interneurons. J Neurophysiol 1999(82): 2476-2489.
[4] Everill B, Rizzo MA, Kocsis JD. Morphologically identified cutaneous afferent DRG neurons express three different potassium currents in varying proportions. J Neurophysiol 1998(79): 1814-1824.
[5] Foehring RC, Surmeier DJ. Voltage-gated potassium currents in acutely dissociated rat cortical neurons. J. Neurophysiolol. 1993, 70: 51-63
[6] Golding NL, Jung HY, Mickus T, Spruston N. Dendritic calcium spike initiation and repolarization are controlled by distinct potassium channel subtypes in CA1 pyramidal neurons. J Neurosci 1999(19): 8789-8798.
[7] Greg M. The puzzling portrait of a pore. Science 2003(300): 2020-2022.
[8] Hille B. Potassium channels and chloride channels. In Ionic Channels of Excitable Membranes (2nd ed.). Sinauer Associates, Sunderland, MA. 1992, p: 116-121.
[9] Jiang QX, Wang DN, MacKinnon R. Electron microscopic analysis of KvAP voltage dependent K~+ channels in an open conformation. Nature 2004(430): 806-810.
[10] Katz B and Miledi R. A re-examination of curare action at the motor endplate. Proc R Soc Lond B Biol Sci 1978 (203): 119-133.
[11] Locke RE, Nerbonne JM. Three kinetically distinct Ca~(2+)-independent depolarization activated K~+ currents in callosa projecting rat visual cortical neurons. J Neurophysiolo 1997(78): 2309-2320.
[12] Malo D, Schurr E, Dorfman J, Canfield V, Levenson R, Gros P. Three brain sodium channel alpha-subunit genes are clustered on the proximal segment of mouse chromosome 2. Genomics. 1991(10): 666-672.
[13] Meech RW. Calcium-mediated potassium activation in Helix neurones. J Physiol 1974 (237): 43-44.
[14] Morita K, North RA and Tokimasa T. Muscarinic agonists inactivate potassium conductance of guinea-pig myenteric neurons. J Physiol (Lond) 1982(333): 125- 139.
[15] Murase K, Ryu PD and Randic M. Substance P augments a persistent slow inward calcium- sensitive current in voltage-clamped spinal dorsal horns of the rat. Brain Res 1986(365): 369-376.
[16] Selyank AA and Sim JA. Ca~(2+)-inhibited non-inactivating K~+ channels in cultured rat hippocampal pyramidal neurons. J Physiol 1998(510): 71-91.
[17] Sheets MF, Kyle, JW, Kallen, RG,Hanck, DA. The Na channel voltage sensor associated with inactivation is localized to the external charged residues of domain IV, S4. Biophys J 1999(77): 747-757.
[18] Sigworth FJ. Life's transistors. Nature 2003(423): 21-22.
[19] Smith RD, Goldin, AL. Phosphorylation at a single site in the rat brain sodium channel is necessary and sufficient for current reduction by protein kinase A. J Neurosci 1997(17): 6086-6093.
[20] Stansfeld C, Feltz A. Dendrotoxin-sensitive K~+ channels in dorsal root ganglion cells. Neurosci Lett 1988(93): 49-55.
[21] Storm J.F. Temporal integration by a slowly inactivating K~+ current in hippocampal neurons. Nature 1988(336): 379-381.
[22] Storm J.F. Functional diversity of K~+ currents in hippocampal pyramidal neurons. SeminNeorusci 1993(5): 79-92.
[23] Stuhmer W, Conti F, Suzuki H, Wang X, Noda M, Yahagi N, Kubo H, Numa S. Structural parts involved in activation and inactivation of sodium channel, Nature 1989(339): 97-603.
[24] Stuhmer W, Conti, F, Suzuki, H, Wang, XD, Noda, M, Yahagi, N, Kubo, H,Numa, S. Structural parts involved in activation and inactivation of the sodium channel. Nature 1989(339): 597-603.
[25] Takeshita Y, Harata N and Akaike N. Suppression of K~+ conductance by metabotropic glutamate receptor in acutely dissociated large cholinergic neurons of rat Caudate Putamen. J Neurophysiol 1996(3): 1545-1558.
[26] West JW, Patton, DE, Scheuer, T, Wang Y, Goldin AL,Catterall WA. A cluster of hydrophobic amino acid residues required for fast Na~+-channel inactivation. Proc Natl Acad Sci USA 1992(89): 10910-10914.
[27] Yang N., George A.L., Horn R., Molecular basis of charge movement in voltage-gated sodium channels, Neuron 1996(16): 113-122.
[28] Youxing Jiang, Alice Lee, Jiayun Chen, Vanessa Ruta, Martine Cadene, Brian T. Chait & Roderick Mackinnon. X-ray structure of a voltage-dependent K~+ channel. Nature 2003(423): 33-41.
[1] Acuna-Castillo C, Morales B, Huidobro-Toro JP. Zinc and copper modulate differentially the P2X4 receptor. J Neurochem 2000(74): 1529-1537.
[2] Allen KG, Klevay LM. Copper deficiency and cholesterol metabolism in the rat. Atherosclerosis 1978(31): 259-271.
[3] Alshuaib WB, Mathew MV. Inhibition of transient K~+ current by copper in Drosophila neurons. Neurochem Res 2004(29): 785-789.
[4] Alt ER, Sternlieb I, Goldfischer S. The cytopathology of metal overload. Int Rev Exp Pathol 1990(31): 165-188.
[5] Andersen PM. Amyotrophic lateral sclerosis associated with mutations in the CuZn superoxide dismutase gene. Curr Neurol Neurosci Rep 2006(6): 37-46.
[6] Arhem P. Effects of some heavy metal ions on the ionic currents of myelinated fibres from Xenopus laevis. J. Physiol. London. 1980(306): 219-231.
[7] Atwood CS, Moir RD, Huang X, Scarpa RC, Bacarra ME, Romano DM, Hartshorn MA, Tanzi RE, Bush AI. Dramatic aggregation of Alzheimer abeta by Cu(II) is induced by conditions representing physiological acidosis. J Biol Chem 1998(273): 12817-12826.
[8] Atwood CS, Scarpa RC, Huang X, Moir RD, Jones WD, Fairlie DP, Tanzi ER, Bush AI. Characterization of copper interactions with Alzheimer amyloid β peptides: identification of an attomolar-affinity copper binding site on amyloid betal-42. J Neurochem 2000(75): 1219-1233.
[9] Baker DH. Czarnecki-Maulden GL. Pharmacologic role of cysteine in ameliorating or exacerbating mineral toxicities. J Nutr 1987(117): 1003-1010.
[10] Bellingham SA, Lahiri DK, Maloney B, La Fontaine S, Multhaup G, Camakaris J. Copper depletion down-regulates expression of the Alzheimer's disease amyloid-beta precursor protein gene. J Biol Chem 2004(279): 20378-20386.
[11] Brewer GJ. Wilson's disease: A clinician's guide to recognition, diagnosis, and management. Boston: Kluwer Academic Publishers, 2001, pp1-27
[12] Britton RS. Metal-induced hepatotoxicity. Semin Liver Dis. 1996(16): 3-12.
[13] Brown DR. Copper and prion diseases. Biochemical Society Transactions 2002(30): 742-745.
[14] Bush AI, The metallobiology of Alzheimer's disease. J Trends Neurosci 2003(26): 207-214.
[15] Cappai R, White AR. Amyloid beta. Int J Biochem Cell Biol 1999(31): 885-889.
[16] Chaoying Li, Robert W. Peoples, Forrest F. Weight. Cu~(2+) potently enhances ATP-activated current in rat nodose. Neurosci Lett 1996 (219): 45-48.
[17] Coddou C, Villalobos C, Gonzalez J, Acuna-Castillo C, Loeb B, Huidobro-Toro JP. Formation of carnosine-Cu(II) complexes prevents and reverts the inhibitory action of copper in P2X4 and P2X7 receptors. J Neurochem 2002(80): 626-633.
[18] Coddou C, Moralesl B, Huidobro-Toro JP. Neuromodulator role of zinc and copper during prolonged ATP applications to P2X4 purinoceptors. Eur J Pharmacol 2003(472): 49-56.
[19] Cohen NL, Keen CL, Lonnerdal B, Hurley LS. Effects of varying dietary iron on the expression of copper deficiency in the growing rat: anemia, ferroxidase I and II, tissue trace elements, ascorbic acid, and exanthine dehydrogenase. J Nutr 1985a(115): 633-649.
[20] Cohen NL, Keen CL, Hurley LS, Lonnerdal B. Determinants of copper-deficiency anemia in rats. J Nutr 1985b(115): 710-725.
[21] Doreulee N, Yanovsky Y, Haas HL. Suppression of long-term potentiation in hippocampal slices by copper. Hippocampus 1997(7): 666-669.
[22] Dorner K, Dziadzka S, Hohn A, Sievers E, Oldigs HD, Schulz-Lell G, Schaub J. Longitudinal manganese and copper balances in young infants and preterm infants fed on breast-milk and adapted cow's milk formulas. Br J Nutr 1989(61): 559-572.
[23] Ehrenkranz RA, Gettner PA, Nelli CM, Sherwonit EA, Williams JE, Ting BTG, Janghorbani M. Zinc and copper nutritional studies in very low birth weight infants: comparison of stable isotopic extrinsic tag and chemical balance methods. Pediatr Res 1989(26): 298-307.
[24] Eide DJ. The molecular biology of metal ion transport in Saccharomyces cerevisiaeAnnu Rev Nutr 1998(18): 44-469.
[25] Sigurdsson EM, Brown DR, Alim MA, Scholtzova H, Carp R, Meeker HC, Prelli F, Frangione B, Wisniewski T. Copper Chelation Delays the Onset of Prion Disease. J Biolo Chem 2003(278): 46199-46202.
[26] El-Youssef M. Wilson disease. Mayo Clin Proc 2003(78): 1126-1136.
[27] Evans GW. Copper homeostasis in the mammalian system. Physiol Rev 1973(53): 535-569.
[28] Fields M, Ferreti RJ, Smith JC Jr, Reiser S. The interaction of type of dietary carbohydrates with copper deficiency. Am J Clin Nutr 1984(39): 289-295.
[29] Fisher JL and Macdonald RL. The role of an alpha subtype M2-M3 His in regulating inhibition of GABAa receptor current by zinc and other divalent cations. J Neurosci 1998(18): 2944-2953.
[30] Goldstein S, Czapski G. The role and mechanism of metal ions and their complexes in enhancing damage in biological systems or in protecting these systems from the toxicity of O2-. J Free Radic Biol Med 1986(2): 3-11.
[31] Gong CX, Lidsky T, Wegiel J, Zuck L, Grundke-Iqbal I, Iqbal K. Phosphorylation of microtubule-associated protein tau is regulated by protein phosphatase 2A in mammalian brain. Implications for neurofibrillary degeneration in Alzheimer's disease. J Biol Chem 2000(275): 5535-5544.
[32] Gur A, Colpan L, Nas K, Cevik R, Sarac J, Erdogan F, Duz MZ. The role of trace minerals in the pathogenesis of postmenopausal osteoporosis and a new effect of calcitonin. J Bone Miner Metab 2002(20): 39-43.
[33] Hamilton IM, Gilmore WS, Strain JJ. Marginal copper deficiency and atherosclerosis. Biol Trace Elem Res 2000(783): 179-189.
[34] Harris ED. Basic and clinical aspects of copper, Crit Rev Clin Lab Sci 2003(40): 547-586.
[35] Hartter D, Barnea A. Evidence for release of copper in the brain: depolarization-induced release of newly taken-up 67copper Synapse 1988(2): 412-415.
[36] Coddou C, Lorca RA, Acuna-Castillo C, Grauso M, Rassendren F, Huidobro-Toro JP. Heavy metals modulate the activity of the purinergic P2X_4 receptor. Toxicol Appl Pharmacol 2005(202): 121-131.
[37] Hermann W, Eggers B, Wagner A. The indication for liver transplant to improve neurological symptoms in a patient with Wilson's disease. J Neurol 2002(249): 1733-1734.
[38] Holdbrook JT, Smith JC Jr, Reiser S. Dietary fructose or starch: effects on copper, zinc, iron, manganese, calcium, and magnesium balances in humans. Am J Clin Nutr 1989(49): 1290-1294.
[39] Horning MS, Trombley PQ. Zinc and copper influence excitability of rat olfactory bulb neurons by multiple mechanisms. J Neurophysiol 2001(86): 1652-1660.
[40] Huang X, Atwood CS, Hartshorn MA, Multhaup G, Goldstein LE, Scarpa RC, Cuajungco MP, Gray DN, Lim J, Moir RD, Tanzi RE, Bush AI. The A beta peptide of Alzheimer's disease directly produces hydrogen peroxide through metal ion reduction. Biochemistry 1999(38): 7609-7616
[41] 金宏伟 ,王晓良,电压依赖性钾通道与人类神经性疾病. 生理科学进展 2002(33): 21-25.
[42] Johnson MA, Murphy CL. Adverse effects of high dietary iron and ascorbic acid on copper status in copper-deficient and copper-adequate rats. Am J Clin Nutr 1988(47): 96-101.
[43] Johnson PE, Korynta ED. Effects of copper, iron, and ascorbic acid on manganese availability to rats. Proc Soc Exp Biol Med 1992(199): 470-480.
[44] Johnson S. Is Parkinson's disease the heterozygote form of Wilson's disease: PD=1/2 WD? Med Hypotheses. 2001(56): 171-173.
[45] Kadrabova J, Madaric A, Sustrova M, Ginter E. Changed serum trace element profile in Down's syndrome Biol Trace Elem Res 1996(54): 201-206.
[46] Kardos J, Kovacs I, Hajos F, Kalman M, Simonyi M. Nerve endings from rat brain tissue release copper upon depolarization. A possible role in regulating neuronal excitability. Neurosci Lett 1989(103): 139-144.
[47] Kim H, Macdonald RL. An N-terminal histidine is the primary determinant of a subunit dependent Cu~(2+) sensitivity of αβ3γ2L GABAa receptors. Mol Pharmacol 2003(64): 1145-1152.
[48] Kitzberger R, Madl C, Ferenci P. Wilson disease. Metab Brain Dis 2005(20): 295-302.
[49] Kowalik-Jankowska T, Ruta-Dolejsz M, Wisniewska K, Lankiewicz L, Kozlowski H. Possible involvement of copper (II) in Alzheimer disease. Environ Health Perspect. 2002(110): (5Suppl): 869s-870s.
[50] Kumar N, Elliott MA, Hoyer JD, Harper CM Jr, Ahlskog JE, Phyliky RL. "Myelodysplasia," myeloneuropathy, and copper deficiency. Mayo Clin Proc 2005(80): 943-946.
[51] Kuwahara C, Takeuchi AM, Nishimura T, Haraguchi K, Kubosaki A, Matsumoto Y, Saeki K, Matsumoto Y, Yokoyama T, Itohara S, Onodera T. Prions prevent neuronal cell-line death. Nature 1999(400): 225-226.
[52] Ladefoged O, Sturup S. Copper deficiency in cattle, sheep and horses caused by excess molybdenum from fly ash: a case report. Vet Hum Toxicol 1995(37): 63-65.
[53] Leiva J, Gaete P, Palestini M. Copper interaction on the long-term potentiation. Arch Ital Biol. 2003(141): 149-155.
[54] Levenson CW. Trace metal regulation of neuronal apoptosis: From genes to behavior. Physiol Beha 86(2005): 399-406.
[55] Li C, Peoples RW, Weight FF. Cu~(2+) potently enhances ATP-activated current in rat nodose ganglion neurons. Neurosci Lett 1996(219): 45-48.
[56] Linder MC. The biochemistry of copper. New York: Plenum Press, 1991.
[57] Liu Y, Liu J, Iszard MB, Andrews GK, Palmiteer RD, Klaassen CD. Transgenic mice that over-express metallothionein-I are protected from cadmium lethality and toxicity. Toxicol Appl Pharmacol 1995(135): 222-228.
[58] Lovell MA, Robertson JD, Teesdale WJ, Campbell JL, Markesbery WR. Copper, iron and zinc in Alzheimer's disease senile plaques. J Neurol Sci 1998(158): 47- 52.
[59] Ma JY, Narahashi T. Differential modulation of GABAa receptor-channel complex by polyvalent cations in rat dorsal root ganglion neurons. Brain Res 1993(607): 222-232.
[60] Marceau N, Aspin N. The intracellular distribution of the radiocopper derived from ceruloplasmin and from albumin. Biochim Biophys Acta 1973a(328): 338-350.
[61] Martin-Lagos F, Navarro-Alarcon M, Terres-Martos C, Lopez-Garcia de la Serrana H, Perez-Valero V, Lopez-Martinez MC. Zinc and copper concentrations in serum from Spanish women during pregnancy. Biol Trace Elem Res 1998(61): 61-70.
[62] Mattson MP. Excitotoxic and excitoprotective mechanisms: abundant targets for the prevention and treatment of neurodegenerative disorders. Neuromolecular Med 2003(3): 65- 94.
[63] Mattson MP. Metal-catalyzed disruption of membrane protein and lipid signaling in the pathogenesis of neurodegenerative disorder. Ann N Y Acad Sci 2004(1012): 37-50.
[64] Miura T, Suzuki K, Kohata N, Takeuchi H. Metal binding modes of Alzheimer's amyloid beta-peptide in insoluble aggregates and soluble complexes. Biochemistry 2000(39): 7024-7031.
[65] Narahashi T, Ma JY, Arakawa O, Reuveny E, and Nakahiro M. GABA receptor-channel complex as a target site of mercury, copper, zinc and lanthanides. Cell Mol Neurobiol 1994(14): 599-621.
[66] Niu ZD, Yu K, Gu Y, Wang M, She JQ, Chen WH, Ruan DY. Effects of copper on A-type potassium currents in acutely dissociated rat hippocampal CA1 neurons. Neuroreport 2005 (16): 1585-1589.
[67] Niu ZD, Wang M, Chen JT, Li XM, Ruan DY. Inhibition of delayed rectifier K~+ currents by copper in acutely dissociated rat hippocampal CA1 neurons. Toxicology Letters, accepted
[68] Nriagu JO ed. Copper in the environment: Part 1. Ecological cycling. New York, John Wiley & Sons Ltd, 1979b, PP43-75.
[69] O'Halloran TV, Culotta VC. Metallochaperones, an Intracellular Shuttle Service for Metal Ions. J Biol Chem 2000(275): 25057-2560.
[70] Owen CA Jr. Metabolism of radio copper (Cu~(64)) in the rat. Am J Physiol 1965(209): 900-904.
[71] Paris I, Dagnino-Subiabre A, Marcelain K, Bennett LB, Caviedes P, Caviedes R, Azar CO, Segura-Aguilar J. Copper neurotoxicity is dependent on dopamine-mediated copper uptake and one-electron reduction of aminochrome in a rat substantia nigra neuronal cell line. J Neurochem 2001(77): 519-529.
[72] Pena MM, Lee J, Thiele DJ. A delicate balance: homeostatic control of copper uptake and distribution. J Nutr 1999(129): 1251-1260.
[73] Pike CJ, Burdick D, Walencewicz AJ, Glabe CG, Cotman CW. Neurodegeneration induced by Neurodegeneration induced by beta-amyloid peptides in vitro: The role of peptide assembly state. J Neurosci 1993(13): 1676-1687.
[74] Reiser S, Smith JC, Mertz W, Holbrook JT, Scholfield DJ, Powell AS, Canfield WK, Canary JJ. Indices in copper status in humans consuming a typical American diet containing either fructose or starch. Am J Clin Nutr 1985(42):242-251.
[75] Robbins KR, Baker DH. Effect of sulfur amino acid level and source on the performance of chicks fed high levels of copper. Poult Sci 1980(59): 1246-1253.
[76] Sayre LM, Perry G, Atwood CS, Smith MA. The role of metals in neurodegenerative disease. Cell Mol Biol 2000(46): 731-741
[77] Sharonova IN, Vorobjev VS, Hass HL. High-affinity copper block of GABAa receptor-mediated currents in acutely isolated cerebellar Purkinje cells of the rat. Eur. J. Neurosci 1998(10): 522-528.
[78] Sharonova IN, Vorobjev VS, Haas HL. Interaction between copper and zinc at GABAa receptors in acutely isolated cerebellar Purkinje cells of the rat. Br J Pharmacol 2000(130): 851-856.
[79] Sliva JRRED, Williams RJP. The Biological Chemistry of the Elements: The Inorganic Chemistry of Life. Oxford: Clarendon Press, 1991.
[80] Soto F, Garcia-Guzman M, Gomez-Hernandez JM, Hollmann M, Karschin C, Stqhmer W. P2X4: an ATP-activated ionotropic receptor cloned from rat brain. Proc Natl Acad Sci USA 1996(93): 3684-3688.
[81] Sparks DL, Schreurs BCT. Trace amounts of copper in water induce β-amyloid plaques and learning deficits in a rabbit model of Alzheimer's disease. J Proc Natl Acad Sci 2003(100): 11065-11069.
[82] Squitti R, Cassetta E, Dal Forno G, Lupoi D, Lippolis G, Pauri F, Vernieri F, Cappa A, Rossini PM. Copper perturbation in 2 monozygotic twins discordant for degree of cognitive impairment. Arch Neurol 2004(61): 738-743.
[83] Sternlieb I. Copper and the liver. Gastroenterology 1980(78): 1615-1628.
[84] Strausak D, Mercer JF, Dieter HH, Stremmel W, Multhaup G. Copper in disorders with neurological symptoms: Alzheimer's, Menkes, and Wilson diseases. Brain Res Bull 2001 (55): 175-185.
[85] Szerdahelyi P, Kasa P. Variation in trace metal levels in rat hippocampus during ontogenetic development. Anat Embryol Berl 1983(167): 141-149.
[86] Szerdahelyi P, Kasa P. Histochemical demonstration of copper in normal rat brain and spinal cord. Evidence of localization in glial cells. Hischemistry 1986(85): 341-347.
[87] Tasaki M, Hanada K, Hashimoto I. Analyses of serum copper and zinc levels and copper/zinc ratios in skin diseases. J Dermatol 1993(20): 21-24.
[88] Thornalley PJ, Vasak M. Possible role for metallothionein in protection against radiation-induced oxidative stress. Kinetics and mechanism of its reaction with superoxide and hydroxyl radicals. Biochim Biophys Acta 1985(827): 36-44.
[89] Ting-Beall HP, Clark DA, Suelter CH, Wells WW. Studies on the interaction of chick brain microsomal (Na~+/ K~+)-ATPase with copper. Biochim Biophys Acta 1973(291): 229-236.
[90] Torsdottir G, Kristinsson J, Hreidarsson S, Snaedal J, Johannesson T. Copper, ceruloplasmin and superoxide dismutase (SOD1) in patients with Down's syndrome. Pharmacol Toxicol 2001(89): 320-325.
[91] Trombley PQ, Shepherd GM. Differential modulation by zinc and copper of amino acid receptors from rat olfactory bulb neurons. J. Neurophysiolo 1996(76): 2088-2094.
[92] Turnlund JR, Swanson CA, King JC. Copper absorption and retention in pregnant women fed diets based on animal and plant proteins. J Nutr 1983(113): 2346-2352.
[93] Turnlund JR. Copper. In: Shils M, Olson JA, Shike M, Ross AC, eds. Nutrition in Health and Disease. 9th ed. Baltimore: Williams & Wilkins; 1999:241-252.
[94] Van den Berg GJ, Beynen AC. Influence of ascorbic acid supplementation on copper metabolism in rats. Br J Nutr 1992(68): 701-715.
[95] VanLandingham JW, Fitch CA, Levenson CW. Zinc inhibits the nuclear translocation of the tumor suppressor protein p53 and protects cultured human neurons from copper induced neurotoxicity. Neuromolecular Med 2002(1): 171- 82.
[96] Varela-Nallar L, Toledo EM, Larrondo LF, Cabral AL, Martins VR, Inestrosa C. Induction of cellular prion protein (PrPC) gene expression by copper in neurons. Am J Physiol Cell Physiol 2006(290): 271-281.
[97] Vasic V, Jovanovic D, Krstic D, Nikezic G, Horvat A, Vujisic L, Nedeljkovic N. Prevention and recovery of CuSO_4induced inhibition of Na~+/K~+-ATPase and Mg~(2+)-ATPase in rat brain synaptosomes by EDTA. Toxicology Letters 110 (1999)95-104
[98] Virginio C, Church D, North RA, Surprenant A. Effects of divalent cations, protons and calmidazolium at the rat P2X_7 receptor. Neuropharmacology 1997(36): 1285-1294.
[99] Vlachova V, Zemkova H, Vyklicky L Jr. Copper modulation of NMDA responses in mouse and rat cultured hippocampal neurons. Eur J Neurosci 1996(8): 2257-2264.
[100] Waggoner DJ, Bartnikas TB, Gitlin JD. The role of copper in neurodegenerative disease. Neurobiol Dis 1999(6): 221-230.
[101] Waggoner DJ, Drisaldi B, Bartnikas TB, Casareno RL, Prohaska JR, Gitlin JD, Harris DA. Brain copper content and cuproenzyme activity do not vary with prion protein expression level. J Biol Chem 2000(275): 7455-7458.
[102] Wang DS, Zhu HL, Hong Z, Li JS. Cu~(2+) inhibition of glycine-activated currents in rat sacral dorsal commissural neurons. Neurosci Lett 2002(328): 117-120.
[103] 王刚 黄振信 祝延，《钾通道功能异常与阿尔茨海默病》。国外医学，老年医学分册 2002(23)：230-232．
[104] 王海鹏，于晓军，何欣，铜与机体防御功能。微量元素与健康研究 2004(21)：58-61
[105] Wang KT. Cu~(2+)induces Ca~(2+)-dependent neurotransmitter release from brain catecholaminergic nerve terminals. Eur J of Pharmacol. 1999(373): 163-169.
[106] 王夔，生命科学中的微量元素[M]。中国计量出版社，1996。
[107] Wapnir RA, Balkman C. Intestinal absorption of copper: influence of carbohydrates. Biochem Med Metab Biol 1992(47): 47-53.
[108] Weiser T, Wienrich M. The effects of copper ions on glutamate receptors in cultured rat cortical neurons. Brain Res. 1996(742): 211-218.
[109] Klein WL, Krafft GA, Finch CE. Targeting small Aβ oligomers: the solution to an Alzheimer's disease conundrum? Trends in Neurosci 2001 (24): 219-224.
[110] Wong BS, Brown DR, Sy MS. A Yin-Yang role for metals in prion disease. Panminerva Med 2001(43): 283-7.
[111] Wong PY, Fritze K. Determination by neutron activation of copper, manganese, and zinc in the pineal body and other areas of brain tissue. J Neurochem 1969; 16: 1231-1234.
[112] 吴茂江，涂长信，微量元素与健康研究。铜与人体健康2005(22)：64-65。
[113] Xie X, Hider RC, Smart TG. Modulation of GABA-mediated synaptic transmission by endogenous zinc in the immature rat hippocampus in vitro. J Physiol (Lond) 1994(478): 75-86.
[114] Xie X, Smart TG. Modulation of long-term potentiation in rat hippocampal pyramidal neurons by zinc. Pfluegers Arch 1994(427): 481-486.
[115] Xiong K, Peoples RW, Montgomery JP, Chiang Y, Stewart RR, Weight FF, Li C. Differential modulation by copper and zinc of P2X2 and P2X4 receptor function. J Neurophysiol 1999(81): 2088-2094.
[116] Yakushiji T, Tokutomi N, Akaike N, Carpenter DO: Antagonists of GABA responses, studied using internally perfused frog dorsal root ganglion neurons. Neuroscience 1987(22): 1123-1133.
[117] Ye CP, Selkoe DJ, Hartley DM. Protofibrils of amyloid beta-protein inhibit specific K~+ currents in neocortical cultures. Neurobiol Dis 2003(13): 177-190.
[1] Alkon DL. Calcium-mediated reduction of ionic currents: A biophysical memory trace. Science 1994(226): 1037-1045.
[2] Alshuaib WB, Mathew MV. Inhibition of transient K~+ current by copper in Drosophila neurons. Neurochem Res 2004(29): 785-789.
[3] Atwood CS, Huang X, Moir RD, Tanzi RE, Bush AI. Role of free radicals and metal ions in the pathogenesis of Alzheimer's disease. Met Ions Biol Syst 1999(36): 309-364.
[4] Atwood CS, Moir RD, Huang X, Scarpa RC, Bacarra ME, Romano DM, Hartshorn MA, Tanzi RE, Bush AI. Dramatic aggregation of Alzheimer abeta by Cu(II) is induced by conditions representing physiological acidosis. J Biol Chem 1998(273): 12817-12826.
[5] Bardoni R, Beluzzi O. Kinetic study and numerical reconstruction of A-type current in granule cells of rat cerebellar slices. J Neurophysiol 1993(69): 222-223.
[6] Brewer GJ. Yusbasian-Gurkan, V. Wilson's disease. Medicine 1992(71): 139-164.
[7] Bush AI. Metals and neuroscience. Curr Opin Chem Biol 2000(4): 184-191.
[8] Chu Chen. β-Amyloid increases dendritic Ca~(2+) influx by inhibiting the A-type K~+ current in hippocampal CA1 pyramidal neurons. Biochemical and Biophysical Research Communications 2005(338): 1913-1919.
[9] Cowan TM, Siegel RW. Drosophila mutations that alter ionic conduction disrupt acquisition and retention of a conditioned odor avoidance response. J. Neurogenet 1986(3): 187-201.
[10] Crow T. Cellular and molecular analysis of associative learning and memory in Hermissenda. Trends Neurosci 1988(11): 136-142.
[11] Debanne D, Guerineau NC,, Gahwiler BH, Thompson SM. Action-potential propagation gated by an axonal I_A-like K~+ conductance in hippocampus. Nature 1997(389): 286-289.
[12] Dedek K, Kunath B, Kananura C, Reuner U, Jentsch TJ, Steinlein OK. Myokymia and neonatal epilepsy caused by a mutation in the voltage sensor of the KCNQ2 K~+ channel. Proc Natl Acad Sci USA. 2001(98): 12272-12277.
[13] Dodart JC, Bales KR, Gannon KS, Greene SJ, DeMattos RB, Mathis C, DeLong CA, Wu S, Wu X, Holtzman DM, Paul SM. Immunization reverses memory deficits without reducing brain Aβ burden in Alzheimer's disease model. Nat Neurosci 2002(5): 452-457.
[14] Fraser SP, Suh YH, Djamgoz MBA. Ionic effects of the Alzheimer's disease β-amyloid precursor protein and its metabolic fragments. Trends Neurosci 1997(20): 67-72.
[15] Giese KP, Storm JF, Reuter D, Fedorov NB, Shao LR, Leicher T, Pongs O, Silva AJ. Reduced K~+ channel inactivation, spike broadening, and after- hyperpolarization in Kvbeta 1.1-deficient mice with impaired learning. Learn Mem. 1998(5): 257-73.
[16] Good TA, Smith DO and Murphy RM. β-Amyloid peptide blocks the fast-inactivating K~+ current in rat hippocampal neurons. Biophys J 1996(70): 296-304.
[17] Hamill, O.P., Marty, A., Neher, E., Sakmann, B., Sigworth, F.J., Improved patch-clamp techniques of high-resolution current recording from cells and cell-free membrane patchs. Pfluegers. Arch. 1981(391): 85-100.
[18] Hardy JA, Higgins GA. Alzheimer's disease: The amyloid cascade hypothesis. Science 1996(256): 184-185.
[19] Hartter D, Barnea A. Evidence for release of copper in the brain: depolarization- induced release of newly taken-up 67copper. Synapse 1988(2): 412-415.
[20] Hartley D, Walsh DM, Ye CP, Diehl T, Vasquez S, Vassilev PM, Teplow DB, Selkoe DJ. Protofibrillar intermediates of amyloid β-protein induce acute electrophysiological changes and progressive neurotoxicity in cortical neurons. J Neurosci 1999(19): 8876-8884.
[21] Hoffman DA, Magee JC, Colbert CM, Johnston D. K~+ channel regulation of signal propagation in dendrites of hippocampal pyramidal neurons. Nature 1997(387): 869-875.
[22] Horning MS, Trombley PQ. Zinc and copper influence excitability of rat olfactory bulb neurons by multiple mechanisms. J Neurophysiol 2001(86): 1652-1660.
[23] Huang X, Cuajungco MP, Atwood CS, Hartshorn MA, Tyndall JD, Hanson GR, Stokes KC, Leopold M, Multhaup G, Goldstein LE, Scarpa RC, Saunders AJ, Lim J, Moir RD, Glabe C, Bowden EF, Masters CL, Fairlie DP, Tanzi RE, Bush AI. Cu(II) potentiation of alzheimer abeta neurotoxicity. Correlation with cell-free hydrogen peroxide production and metal reduction. J Biol Chem 1999 (274): 3111-37116.
[24] Kaczmarek LK. Voltage-dependent potassium channels: minK and Shaker families. New Biol 1991(3): 315-323.
[25] Kaneda M, Nakamura H, Akaike N. Mechanism and enzymatic isolation of mammalian CNS neurons. Neurosci. Res. 1988(5): 299-315.
[26] Kardos J, Kovacs I, Hajos F, Kalman M, Simonyi M. Nerve endings from rat brain tissue release copper upon depolarization. A possible role in regulating neuronal excitability. Neurosci Lett 1989(103): 139-144.
[27] Kubisch C, Schroeder BC, Friedrich T, Lutjohann B, El-Amraoui A, Marlin S, Petit C, Jentsch TJ. KCNQ4, a novel potassium channel expressed in sensory outer hair cells, is mutated in dominant deafness. Cell 1999(5): 437-446.
[28] Lambert MP, Barlow AK, Chromy BA, Edwards C, Freed R, iosatos M, Morgan TE, Rozovsky I, Trommer B, Viola KL, Wals P, Zhang C, Finch CE, Kraff, GA, Klein WL, Diffusible, nonfribrillar ligands derived from Aβ1-42 are potent central nervous system neurotoxins. Proc Natl Acad Sci USA 1998(95): 6448-6453.
[29] LeMasson G, Marder E, Abbott LF. Activity-dependent regulation of conductances in model neurons. Science 1993(259): 1915-1917.
[30] Lorenzo A, Yankner BA. β-Amyloid neurotoxicity requires fibril formation and is inhibited by Congo red. Proc Natl Acad Sci USA 1994(91): 12243-12247.
[31] Lovell M A, Robertson J D, Teesdale W J, Campbell J L, Markesbery WR. Copper, iron and zinc in Alzheimer's disease senile plaques. J Neurol Sci 1998(158): 47-52.
[32] Lutsenko S, Petris MJ. Function and regulation of the mammalian copper-transporting ATPases: insights from biochemical and cell biological approaches. J Membr Biol 2003(191): 1-12.
[33] Ma M, J Koester. The role of K~+ currents in frequency-dependent spike broadening in Aplysia R20 neurons: A dynamic-clamp analysis. J Neurosci 1996(16): 4089-4101.
[34] Maynard CJ, Cappai R, Volitakis I, Cherny RA, White AR, Beyreuther K, Masters CL, Bush AI, Li QX. Overexpression of Alzheimer's disease amyloid-beta opposes the age-dependent elevations of brain copper and iron. J Biol Chem. 2002(277):44670-44676.
[35] Murase K, Ryu PD, Randic M. Excitatory and inhibitory amino acids and peptide-induced responses in acutely isolated rat spinal dorsal horn neurons. Neurosci Lett. 1989(103): 56-63.
[36] Okeda R, Gei S, Chen I, Okaniwa M, Shinomiya M, Matsubara O, Menkes' kinky hair disease: morphological and immunohistochemical comparison of two autopsied patients. Acta Neuropathol (Berl) 1991(81): 450-457.
[37] Pike CJ, Burdick D, Walencewicz AJ, Glabe CG, Cotman CW. Neurodegeneration induced by Neurodegeneration induced by β-amyloid peptides in vitro: The role of peptide assembly state. J Neurosci 1993(13): 1676-1687.
[38] Roeper J, O Pongs. Presynaptic potassium channels. Curr Opin Neurobiol 1996(6): 338-341.
[39] Rudy B. Diversity and ubiquity of K channels. Neurosci 1988(25): 729-749.
[40] Shirasaki T, Klee MR, Nakaye T, Akaike N. Differential blockade of bicuculline and strychnine on GABA- and glycine-induced responses in dissociated rat hippocampal pyramidal cells. Brain Res. 1991(561): 77-83.
[41] Southan AP, Robertson BJ. Patch-clamp recordings from cerebellar basket cell bodies and their presynaptic terminals reveal an asymmetric distribution of voltage-gated potassium channels. Neurosci 1998(18): 948-955.
[41] Sparks DL, Schreurs BG. Trace amounts of copper in water induce P-amyloid plaques and learning deficits in a rabbit model of Alzheimer's disease. Proc Natl Acad Sci USA 2003(100): 11065-11069.
[42] Storm JF. Action potential repolarization and a fast fter-hyperpolarization in rat hippocampal pyramidal cells. J Physiol (Lond) 1987(385): 733-759.
[43] Szerdahelyi P, Kasa P. Variation in trace metal levels in rat hippocampus during ontogenetic development. Anat Embryol Berl 1983(167):141-149.
[44] Szerdahelyi P, Kasa P. Histochemical demonstration of copper in normal rat brain and spinal cord. Evidence of localization in glial cells. Hischemistry 1986(85): 341-347.
[45] Wang HW, Pasternak JF, Kuo H, Ristic H, Lambert MP, Chromy B, Viola KL, Klein WL, Stine WB, Krafft GA, Trommer BL, Soluble oligomers of beta amyloid (1-42) inhibit long-term potentiation but not long-term depression in rat dentate gyrus. Brain Res 2002(924): 133-140.
[46] Wong PY, Fritze K. Determination by neutron activation of copper, manganese, and zinc in the pineal body and other areas of brain tissue. J Neurochem 1969(16): 1231-1234.
[1] Alshuaib WB, Mathew MV. Inhibition of transient K~+ current by copper in Drosophila neurons. Neurochem Res 2004(29) 785-789.
[2] Arhem P. Effects of some heavy metal ions on the ionic currents of myelinated fibres from Xenopus laevis. J. Physiol London 1980(306): 219-231.
[3] Assaf SY, Chung SH, Release of endogenous Zn~(2+) from brain tissue during activity. Nature 1984(308): 734-736.
[4] Bayer TA, Schafer S, Simons A, Kemmling A, Kamer T, Tepest R, Eckert A, Schussel K, Eikenberg O, Sturchler-Pierrat C, Abramowski D, Staufenbiel M, Multhaup G, Dietary Cu stabilizes brain superoxide dismutase 1 activity and reduces amyloid Aβ production in APP23 transgenic mice Proc Natl Acad Sci USA 2003(100): 14187-14192.
[5] Beckman JS. Peroxynitrite versus hydroxyl radical: the role of nitric oxide in superoxide-dependent cerebral injury. Ann N Y Acad Sci 1994(738): 382-387.
[6] Brewer GJ, Yusbasian-Gurkan V. Wilson's disease. Medicine 1992(71): 139-164.
[7] Brown DR. Copper and prion disease. Brain Res Bull 2001(55): 165-173.
[8] Bull PC, Cox DW. Wilson disease and Menkes disease: new handles on heavy-metal transport. Trends Genet. 1994(10): 246-252.
[9] Coddou C, Moralesl B, Huidobro-Toro JP. Neuromodulator role of zinc and copper during prolonged ATP applications to P2X_4 purinoceptors. Eur. J. Pharmacol. 2003(472): 49- 56.
[10] Hamill, OP, Marty A, Neher E, Sakmann B, Sigworth FJ. Improved patch-clamp techniques of high-resolution current recording from cells and cell-free membrane patchs. Pfluegers. Arch. 1981(391): 85-100.
[11] Saito T, Okabe M, Hosokawa T, Kurasaki M, Hata A, Endo F, Nagano K, Matsuda I, Urakami K, Saito K. Immunohistochemical determination of the Wilson Coppertransporting P-type ATPase in the brain tissues of the rat. Neurosci. Lett. 1999(266): 13-16.
[12] Horning MS, Trombley PQ. Zinc and copper influence excitability of rat olfactory bulb neurons by multiple mechanisms. J. Neurophysiol. 2001(86): 1652-1660.
[13] Hui K, Davis BA, Boulton AA. Analysis of copper in brain by the masspectrometric-integrated-ion-current procedure. Neurochem. Res. 1987(2): 495-506.
[14] Kaneda M, Nakamura H, Akaike N. Mechanism and enzymatic isolation of mammalian CNS neurons. Neurosci. Res. 1988(5): 299-315.
[15] Kardos J, Kovacs I, Hajos F, Kalman M, Simonyi M. Nerve endings from rat brain tissue release copper upon depolarization. A possible role in regulating neuronal excitability. Neurosci. Lett. 1989(103): 139-144.
[16] Kim H, Macdonald RL. An N-terminal histidine is the primary determinant of a subunit-dependent Cu~(2+) sensitivity of αβ3γ2L GABAa receptors. Mol. Pharmacol. 2003(64): 1145-1152.
[17] Kues WA, Wunder F. Heterogeneous expression patterns of mammalian potassium channel genes in developing and adult rat brain. Eur. J. Neurosci. 1992(4):1296-1308.
[18] LeMasson G, Marder E, Abbott LF. Activity-dependent regulation of conductances in model neurons. Science. 1993(259): 1915-1917.
[19] Li C, Peoples RW, Weight FF. Cu~(2+) potently enhances ATP-activated current in rat nodose ganglion neurons. Neurosci. Lett. 1996(219): 45-48.
[20] Lutsenko S, Cooper MJ. Localization of the Wilson's disease protein product to mitochondria. Proc. Natl. Acad. Sci. U. S. A. 1998(95): 6004-6009.
[21] Nalbandyan RM. Copper in brain. Neurochem. Res. 1983(8):1211-1232.
[22] Niu ZD, Yu K, Gu Y, Wang M, She JQ, Chen WH, Ruan DY. Effects of copper on A-type potassium currents in acutely dissociated rat hippocampal CA1 neurons. Neuroreport, 2005(16): 1585-1589.
[23] Okeda R, Gei S, Chen I, Okaniwa M, Shinomiya M, Matsubara O. Menkes' kinky hair disease: morphological and immunohistochemical comparison of two autopsied patients. Acta Neuropathol. Berl. 1991(81): 450-457.
[24] Olivares M, Uauy R. Copper as an essential nutrient. Am. J. Clin. Nutr. 1996(63): (Suppl.), 791S-796S.
[25] Phinney AL, Drisaldi B, Schmidt SD, Lugowski S, Coronado V, Liang Y, Home P, Yang J, Sekoulidis J, Coomaraswamy J, Chishti MA, Cox DW, Mathews PM, Nixon RA, Carlson GA, St George-Hyslop P, Westaway D. In vivo reduction of amyloid-β by a mutant copper transporter, Proc. Natl. Acad. Sci. U.S.A. 2003(100): 14193-14198.
[26] Saito T, Okabe M, Hosokawa T, Kurasaki M, Hata A, Endo F, Nagano K, Matsuda I, Urakami K, Saito K. Immunohistochemical determination of the Wilson Copper transporting P-type ATPase in the brain tissues of the rat. Neurosci Lett. 1999(266): 13-16.
[27] Scheinberg IH, Sternlieb I. Wilson's disease. In: Smith LH Jr, editor. Major problems in internal medicine 1984(23): Philadelphia: WB Saunders Co.
[28] Sharonova IN, Vorobjev VS, Hass HL. High-affinity copper block of GABA_A receptor-mediated currents in acutely isolated cerebellar Purkinje cells of the rat. Eur. J. Neurosci. 1998(10): 522-528.
[29] Sheline CT, Choi EH, Kim-Han JS, Dugan LL, Choi DW. Cofactors of mitochondrial enzymes attenuate copper-induced death in vitro and in vivo. Ann. Neurol. 2002(52): 195-204.
[30] Simonian NA, Coyle JT. Oxidative stress in neurodegenerative diseases. Annu. Rev. Pharmacol. Toxicol. 1996(36): 83-106.
[31] Sorenson RJ. Prion diseases: copper deficiency states associated with impaired nitrogen monoxide or carbon monoxide transduction and translocation. J.Inorg. Biochem. 2001 ( 87): 125-127.
[32] Sparks DL, Schreurs BG. Trace amounts of copper in water induce β-amyloid plaques and learning deficits in a rabbit model of Alzheimer's disease. Proc. Natl. Acad. Sci. U.S.A. 2003(100): 11065-11069.
[33] Trombley PQ, Shepherd GM. Differential modulation by zinc and copper of amino acid receptors from rat olfactory bulb neurons. J. Neurophysiolo. 1996(76): 2088-2094.
[34] Vlachova V, Zemkova H, Vyklicky LJr. Copper modulation of NMD A responses in mouse and rat cultured hippocampal neurons. Eur. J. Neurosci. 1996(8): 2257-2264.
[35] Wang DS, Zhu HL, Hong Z, Li JS. Cu~(2+) inhibition of glycine-activated currents in rat sacral dorsal commissural neurons. Neurosci Lett. 2002(328): 117-120.
[36] Wang KT. Cu~(2+) induces Ca~(2+)-dependent neurotransmitter release from brain catecholaminergic nerve terminals. European J of Pharmacology. 1999(373): 163-169.
[37] Weiser T, Wienrich M. The effects of copper ions on glutamate receptors in cultured rat cortical neurons. Brain Res. 1996(742): 211-218.
[38] Yost CS. Potassium channels: basic aspects, functional roles, and medical significance, Anesthesiology. 1999(90): 1186-1203.
[2] Barinaga M. Is nitric oxide the "retrograde messenger"? Science 1991(254): 1296-1297.
[3] Bear MF, Dudek SM and Gold JT. Homosynaptic long-term depression in CA1 of rat hippocampus in vitro. Soc. Neurosci Abstr 1992(17): 533.
[4] Berger TW. Long-term potentiation of hippocampal synaptic transmission affects rate of behavioral leaming. Science 1984(224): 627-630.
[5] Bliss TV. Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path. J Physiol 1973(232): 331-356.
[6] Bliss TV and Collibgridge GL. A synaptic model of memory: long-term potentiation in the hippocampus. Nature, 1993, 361:31-39.
[7] Giese KP, Storm JF, Reuter D, Fedorov NB, Shao LR, Leicher T, Pongs O and Silva AJ. Reduced K~+ channel inactivation, spike broadening, and after hyperpolarization in Kvβ 1.1-deficient mice with impaired learning. Learn Mere 1998(5): 257-273.
[8] Giese KP, Peters M, Vemon J. Modulation of excitability as a learning and memory mechanism: A molecular genetic perspective. Physiol Behav 2001(73): 803-810.
[9] 韩太真、吴馥梅主编，学习与记忆的神经生物学。北京医科大学、中国协和大学联合出版社 1998。
[10] Hebb DO. The organization of behavior. Wiley, New York, 1949.
[11] Huang SC, Carson RE, Hoffman EJ, Kuhl DE, Phelps ME. An investigation of a doubletracer technique for positron computerized tomography. J Nucl Med 1982(23): 816-822.
[12] Huerta PT, Lisman JE. Synaptic plasticity during the cholinergic theta- frequency oscillation in vitro. Hippocampus 1996(6): 58-61.
[13] Ito M. Long-term depression. Ann. Rev. Neurosci., 1989, 12: 85-102.
[14] 蒋文，肖鹏，徐世彤。齿状回习得性LTP的形成与θ节律的变化。生理学报 1995(12)：67．
[15] Kirkwood A, Rioult M and Bear MF. Experience-dependent modification of synaptic plastiity in visual cortex. Nature 1996(381): 526-528.
[16] Linden DJ and Connor JA. Long-term depression. Ann Rev Neurosci 1995(18): 319- 357.
[17] Lomon T. Frequence potentiation of excitatory synaptic activity in the dentate area of the hippocampal formation. Acta physiol Scond 1996(68) ( supp 1): 277.
[18] MacVinish LJ, Guo Y, Dixon AK, Murrell-Lagnado, RD, Cuthbert, AW. XE991 reveals differences in K~+ channels regulating chloride secretion in murine airway and colonic epithelium. Mol Pharmacol 2001(60): 753-760.
[19] Orr G, Rao G, Houston FP, McNaughton BL, Barnes CA. Hippocampal synaptic plasticity is modulated by theta rhythm in the fascia dentata of adult and aged freely behaving rats. Hippocampus 2001(11): 647-654.
[20] Racine RJ, Milgram NW and Hafner S. Long-term potentiation phenomena in the rat limbic forebrain. Brain Res 1983(260): 217-232.
[21] Ranck JB Jr. Studies on single neurons in dorsal hippocampal formation and septum in unrestrained rats. I. Behavioral correlates and firing repertoires. Exp Neurol 1973(41): 461-531.
[22] Sato N, Yamaguchi Y. Memory encoding by theta phase precession in the hippocampal net work. Neural Comput 2003(15): 2379-2397.
[23] Scoville WB and Milner B. Loss of recent memory after bilateral hippocampal lesions. J Neurol Neurosurg Psych 1957(20): 11-21.
[24] Watabe AM, O'Dell TJ. Age-related changes in theta frequency stimulation-induced long-term potentiation. Neurobiol Aging 2003(24): 267-272.
[25] Watkins JC and Evans RH. Excitatory amino acid transmitters. Ann Rev Pharmacol Toxicol 1981(21): 165-204.
[26] 吴馥梅，萧信生。学习记忆及其脑内突触机制。自然杂志199l(14)：746-751．
[1] Chabbertet C, Chambard JM, Sans A, Desmadryl G. Three types of depolarization-activated potassium currents in acutely isolated mouse vestibular neurons. J Neurophysiol 2001(85): 1017-1026.
[2] Coetzee WA, Amarillo Y, Chiu J, Chow A, Lau D, McCormack T, Moreno H, Nadal MS, Ozaita A, Pountney D, Saganich M, Vega-Saenz de Miera E, Rudy B. Molecular diversity of K~+ channels. Ann NY Acad Sci 1993(868): 233-285.
[3] Erisir A., Lau D., Rudy B., Leonard C.S. Function of specific K~+ channels in sustained high frequency firing of fast-spiking neocortical interneurons. J Neurophysiol 1999(82): 2476-2489.
[4] Everill B, Rizzo MA, Kocsis JD. Morphologically identified cutaneous afferent DRG neurons express three different potassium currents in varying proportions. J Neurophysiol 1998(79): 1814-1824.
[5] Foehring RC, Surmeier DJ. Voltage-gated potassium currents in acutely dissociated rat cortical neurons. J. Neurophysiolol. 1993, 70: 51-63
[6] Golding NL, Jung HY, Mickus T, Spruston N. Dendritic calcium spike initiation and repolarization are controlled by distinct potassium channel subtypes in CA1 pyramidal neurons. J Neurosci 1999(19): 8789-8798.
[7] Greg M. The puzzling portrait of a pore. Science 2003(300): 2020-2022.
[8] Hille B. Potassium channels and chloride channels. In Ionic Channels of Excitable Membranes (2nd ed.). Sinauer Associates, Sunderland, MA. 1992, p: 116-121.
[9] Jiang QX, Wang DN, MacKinnon R. Electron microscopic analysis of KvAP voltage dependent K~+ channels in an open conformation. Nature 2004(430): 806-810.
[10] Katz B and Miledi R. A re-examination of curare action at the motor endplate. Proc R Soc Lond B Biol Sci 1978 (203): 119-133.
[11] Locke RE, Nerbonne JM. Three kinetically distinct Ca~(2+)-independent depolarization activated K~+ currents in callosa projecting rat visual cortical neurons. J Neurophysiolo 1997(78): 2309-2320.
[12] Malo D, Schurr E, Dorfman J, Canfield V, Levenson R, Gros P. Three brain sodium channel alpha-subunit genes are clustered on the proximal segment of mouse chromosome 2. Genomics. 1991(10): 666-672.
[13] Meech RW. Calcium-mediated potassium activation in Helix neurones. J Physiol 1974 (237): 43-44.
[14] Morita K, North RA and Tokimasa T. Muscarinic agonists inactivate potassium conductance of guinea-pig myenteric neurons. J Physiol (Lond) 1982(333): 125- 139.
[15] Murase K, Ryu PD and Randic M. Substance P augments a persistent slow inward calcium- sensitive current in voltage-clamped spinal dorsal horns of the rat. Brain Res 1986(365): 369-376.
[16] Selyank AA and Sim JA. Ca~(2+)-inhibited non-inactivating K~+ channels in cultured rat hippocampal pyramidal neurons. J Physiol 1998(510): 71-91.
[17] Sheets MF, Kyle, JW, Kallen, RG,Hanck, DA. The Na channel voltage sensor associated with inactivation is localized to the external charged residues of domain IV, S4. Biophys J 1999(77): 747-757.
[18] Sigworth FJ. Life's transistors. Nature 2003(423): 21-22.
[19] Smith RD, Goldin, AL. Phosphorylation at a single site in the rat brain sodium channel is necessary and sufficient for current reduction by protein kinase A. J Neurosci 1997(17): 6086-6093.
[20] Stansfeld C, Feltz A. Dendrotoxin-sensitive K~+ channels in dorsal root ganglion cells. Neurosci Lett 1988(93): 49-55.
[21] Storm J.F. Temporal integration by a slowly inactivating K~+ current in hippocampal neurons. Nature 1988(336): 379-381.
[22] Storm J.F. Functional diversity of K~+ currents in hippocampal pyramidal neurons. SeminNeorusci 1993(5): 79-92.
[23] Stuhmer W, Conti F, Suzuki H, Wang X, Noda M, Yahagi N, Kubo H, Numa S. Structural parts involved in activation and inactivation of sodium channel, Nature 1989(339): 97-603.
[24] Stuhmer W, Conti, F, Suzuki, H, Wang, XD, Noda, M, Yahagi, N, Kubo, H,Numa, S. Structural parts involved in activation and inactivation of the sodium channel. Nature 1989(339): 597-603.
[25] Takeshita Y, Harata N and Akaike N. Suppression of K~+ conductance by metabotropic glutamate receptor in acutely dissociated large cholinergic neurons of rat Caudate Putamen. J Neurophysiol 1996(3): 1545-1558.
[26] West JW, Patton, DE, Scheuer, T, Wang Y, Goldin AL,Catterall WA. A cluster of hydrophobic amino acid residues required for fast Na~+-channel inactivation. Proc Natl Acad Sci USA 1992(89): 10910-10914.
[27] Yang N., George A.L., Horn R., Molecular basis of charge movement in voltage-gated sodium channels, Neuron 1996(16): 113-122.
[28] Youxing Jiang, Alice Lee, Jiayun Chen, Vanessa Ruta, Martine Cadene, Brian T. Chait & Roderick Mackinnon. X-ray structure of a voltage-dependent K~+ channel. Nature 2003(423): 33-41.
[1] Acuna-Castillo C, Morales B, Huidobro-Toro JP. Zinc and copper modulate differentially the P2X4 receptor. J Neurochem 2000(74): 1529-1537.
[2] Allen KG, Klevay LM. Copper deficiency and cholesterol metabolism in the rat. Atherosclerosis 1978(31): 259-271.
[3] Alshuaib WB, Mathew MV. Inhibition of transient K~+ current by copper in Drosophila neurons. Neurochem Res 2004(29): 785-789.
[4] Alt ER, Sternlieb I, Goldfischer S. The cytopathology of metal overload. Int Rev Exp Pathol 1990(31): 165-188.
[5] Andersen PM. Amyotrophic lateral sclerosis associated with mutations in the CuZn superoxide dismutase gene. Curr Neurol Neurosci Rep 2006(6): 37-46.
[6] Arhem P. Effects of some heavy metal ions on the ionic currents of myelinated fibres from Xenopus laevis. J. Physiol. London. 1980(306): 219-231.
[7] Atwood CS, Moir RD, Huang X, Scarpa RC, Bacarra ME, Romano DM, Hartshorn MA, Tanzi RE, Bush AI. Dramatic aggregation of Alzheimer abeta by Cu(II) is induced by conditions representing physiological acidosis. J Biol Chem 1998(273): 12817-12826.
[8] Atwood CS, Scarpa RC, Huang X, Moir RD, Jones WD, Fairlie DP, Tanzi ER, Bush AI. Characterization of copper interactions with Alzheimer amyloid β peptides: identification of an attomolar-affinity copper binding site on amyloid betal-42. J Neurochem 2000(75): 1219-1233.
[9] Baker DH. Czarnecki-Maulden GL. Pharmacologic role of cysteine in ameliorating or exacerbating mineral toxicities. J Nutr 1987(117): 1003-1010.
[10] Bellingham SA, Lahiri DK, Maloney B, La Fontaine S, Multhaup G, Camakaris J. Copper depletion down-regulates expression of the Alzheimer's disease amyloid-beta precursor protein gene. J Biol Chem 2004(279): 20378-20386.
[11] Brewer GJ. Wilson's disease: A clinician's guide to recognition, diagnosis, and management. Boston: Kluwer Academic Publishers, 2001, pp1-27
[12] Britton RS. Metal-induced hepatotoxicity. Semin Liver Dis. 1996(16): 3-12.
[13] Brown DR. Copper and prion diseases. Biochemical Society Transactions 2002(30): 742-745.
[14] Bush AI, The metallobiology of Alzheimer's disease. J Trends Neurosci 2003(26): 207-214.
[15] Cappai R, White AR. Amyloid beta. Int J Biochem Cell Biol 1999(31): 885-889.
[16] Chaoying Li, Robert W. Peoples, Forrest F. Weight. Cu~(2+) potently enhances ATP-activated current in rat nodose. Neurosci Lett 1996 (219): 45-48.
[17] Coddou C, Villalobos C, Gonzalez J, Acuna-Castillo C, Loeb B, Huidobro-Toro JP. Formation of carnosine-Cu(II) complexes prevents and reverts the inhibitory action of copper in P2X4 and P2X7 receptors. J Neurochem 2002(80): 626-633.
[18] Coddou C, Moralesl B, Huidobro-Toro JP. Neuromodulator role of zinc and copper during prolonged ATP applications to P2X4 purinoceptors. Eur J Pharmacol 2003(472): 49-56.
[19] Cohen NL, Keen CL, Lonnerdal B, Hurley LS. Effects of varying dietary iron on the expression of copper deficiency in the growing rat: anemia, ferroxidase I and II, tissue trace elements, ascorbic acid, and exanthine dehydrogenase. J Nutr 1985a(115): 633-649.
[20] Cohen NL, Keen CL, Hurley LS, Lonnerdal B. Determinants of copper-deficiency anemia in rats. J Nutr 1985b(115): 710-725.
[21] Doreulee N, Yanovsky Y, Haas HL. Suppression of long-term potentiation in hippocampal slices by copper. Hippocampus 1997(7): 666-669.
[22] Dorner K, Dziadzka S, Hohn A, Sievers E, Oldigs HD, Schulz-Lell G, Schaub J. Longitudinal manganese and copper balances in young infants and preterm infants fed on breast-milk and adapted cow's milk formulas. Br J Nutr 1989(61): 559-572.
[23] Ehrenkranz RA, Gettner PA, Nelli CM, Sherwonit EA, Williams JE, Ting BTG, Janghorbani M. Zinc and copper nutritional studies in very low birth weight infants: comparison of stable isotopic extrinsic tag and chemical balance methods. Pediatr Res 1989(26): 298-307.
[24] Eide DJ. The molecular biology of metal ion transport in Saccharomyces cerevisiaeAnnu Rev Nutr 1998(18): 44-469.
[25] Sigurdsson EM, Brown DR, Alim MA, Scholtzova H, Carp R, Meeker HC, Prelli F, Frangione B, Wisniewski T. Copper Chelation Delays the Onset of Prion Disease. J Biolo Chem 2003(278): 46199-46202.
[26] El-Youssef M. Wilson disease. Mayo Clin Proc 2003(78): 1126-1136.
[27] Evans GW. Copper homeostasis in the mammalian system. Physiol Rev 1973(53): 535-569.
[28] Fields M, Ferreti RJ, Smith JC Jr, Reiser S. The interaction of type of dietary carbohydrates with copper deficiency. Am J Clin Nutr 1984(39): 289-295.
[29] Fisher JL and Macdonald RL. The role of an alpha subtype M2-M3 His in regulating inhibition of GABAa receptor current by zinc and other divalent cations. J Neurosci 1998(18): 2944-2953.
[30] Goldstein S, Czapski G. The role and mechanism of metal ions and their complexes in enhancing damage in biological systems or in protecting these systems from the toxicity of O2-. J Free Radic Biol Med 1986(2): 3-11.
[31] Gong CX, Lidsky T, Wegiel J, Zuck L, Grundke-Iqbal I, Iqbal K. Phosphorylation of microtubule-associated protein tau is regulated by protein phosphatase 2A in mammalian brain. Implications for neurofibrillary degeneration in Alzheimer's disease. J Biol Chem 2000(275): 5535-5544.
[32] Gur A, Colpan L, Nas K, Cevik R, Sarac J, Erdogan F, Duz MZ. The role of trace minerals in the pathogenesis of postmenopausal osteoporosis and a new effect of calcitonin. J Bone Miner Metab 2002(20): 39-43.
[33] Hamilton IM, Gilmore WS, Strain JJ. Marginal copper deficiency and atherosclerosis. Biol Trace Elem Res 2000(783): 179-189.
[34] Harris ED. Basic and clinical aspects of copper, Crit Rev Clin Lab Sci 2003(40): 547-586.
[35] Hartter D, Barnea A. Evidence for release of copper in the brain: depolarization-induced release of newly taken-up 67copper Synapse 1988(2): 412-415.
[36] Coddou C, Lorca RA, Acuna-Castillo C, Grauso M, Rassendren F, Huidobro-Toro JP. Heavy metals modulate the activity of the purinergic P2X_4 receptor. Toxicol Appl Pharmacol 2005(202): 121-131.
[37] Hermann W, Eggers B, Wagner A. The indication for liver transplant to improve neurological symptoms in a patient with Wilson's disease. J Neurol 2002(249): 1733-1734.
[38] Holdbrook JT, Smith JC Jr, Reiser S. Dietary fructose or starch: effects on copper, zinc, iron, manganese, calcium, and magnesium balances in humans. Am J Clin Nutr 1989(49): 1290-1294.
[39] Horning MS, Trombley PQ. Zinc and copper influence excitability of rat olfactory bulb neurons by multiple mechanisms. J Neurophysiol 2001(86): 1652-1660.
[40] Huang X, Atwood CS, Hartshorn MA, Multhaup G, Goldstein LE, Scarpa RC, Cuajungco MP, Gray DN, Lim J, Moir RD, Tanzi RE, Bush AI. The A beta peptide of Alzheimer's disease directly produces hydrogen peroxide through metal ion reduction. Biochemistry 1999(38): 7609-7616
[41] 金宏伟 ,王晓良,电压依赖性钾通道与人类神经性疾病. 生理科学进展 2002(33): 21-25.
[42] Johnson MA, Murphy CL. Adverse effects of high dietary iron and ascorbic acid on copper status in copper-deficient and copper-adequate rats. Am J Clin Nutr 1988(47): 96-101.
[43] Johnson PE, Korynta ED. Effects of copper, iron, and ascorbic acid on manganese availability to rats. Proc Soc Exp Biol Med 1992(199): 470-480.
[44] Johnson S. Is Parkinson's disease the heterozygote form of Wilson's disease: PD=1/2 WD? Med Hypotheses. 2001(56): 171-173.
[45] Kadrabova J, Madaric A, Sustrova M, Ginter E. Changed serum trace element profile in Down's syndrome Biol Trace Elem Res 1996(54): 201-206.
[46] Kardos J, Kovacs I, Hajos F, Kalman M, Simonyi M. Nerve endings from rat brain tissue release copper upon depolarization. A possible role in regulating neuronal excitability. Neurosci Lett 1989(103): 139-144.
[47] Kim H, Macdonald RL. An N-terminal histidine is the primary determinant of a subunit dependent Cu~(2+) sensitivity of αβ3γ2L GABAa receptors. Mol Pharmacol 2003(64): 1145-1152.
[48] Kitzberger R, Madl C, Ferenci P. Wilson disease. Metab Brain Dis 2005(20): 295-302.
[49] Kowalik-Jankowska T, Ruta-Dolejsz M, Wisniewska K, Lankiewicz L, Kozlowski H. Possible involvement of copper (II) in Alzheimer disease. Environ Health Perspect. 2002(110): (5Suppl): 869s-870s.
[50] Kumar N, Elliott MA, Hoyer JD, Harper CM Jr, Ahlskog JE, Phyliky RL. "Myelodysplasia," myeloneuropathy, and copper deficiency. Mayo Clin Proc 2005(80): 943-946.
[51] Kuwahara C, Takeuchi AM, Nishimura T, Haraguchi K, Kubosaki A, Matsumoto Y, Saeki K, Matsumoto Y, Yokoyama T, Itohara S, Onodera T. Prions prevent neuronal cell-line death. Nature 1999(400): 225-226.
[52] Ladefoged O, Sturup S. Copper deficiency in cattle, sheep and horses caused by excess molybdenum from fly ash: a case report. Vet Hum Toxicol 1995(37): 63-65.
[53] Leiva J, Gaete P, Palestini M. Copper interaction on the long-term potentiation. Arch Ital Biol. 2003(141): 149-155.
[54] Levenson CW. Trace metal regulation of neuronal apoptosis: From genes to behavior. Physiol Beha 86(2005): 399-406.
[55] Li C, Peoples RW, Weight FF. Cu~(2+) potently enhances ATP-activated current in rat nodose ganglion neurons. Neurosci Lett 1996(219): 45-48.
[56] Linder MC. The biochemistry of copper. New York: Plenum Press, 1991.
[57] Liu Y, Liu J, Iszard MB, Andrews GK, Palmiteer RD, Klaassen CD. Transgenic mice that over-express metallothionein-I are protected from cadmium lethality and toxicity. Toxicol Appl Pharmacol 1995(135): 222-228.
[58] Lovell MA, Robertson JD, Teesdale WJ, Campbell JL, Markesbery WR. Copper, iron and zinc in Alzheimer's disease senile plaques. J Neurol Sci 1998(158): 47- 52.
[59] Ma JY, Narahashi T. Differential modulation of GABAa receptor-channel complex by polyvalent cations in rat dorsal root ganglion neurons. Brain Res 1993(607): 222-232.
[60] Marceau N, Aspin N. The intracellular distribution of the radiocopper derived from ceruloplasmin and from albumin. Biochim Biophys Acta 1973a(328): 338-350.
[61] Martin-Lagos F, Navarro-Alarcon M, Terres-Martos C, Lopez-Garcia de la Serrana H, Perez-Valero V, Lopez-Martinez MC. Zinc and copper concentrations in serum from Spanish women during pregnancy. Biol Trace Elem Res 1998(61): 61-70.
[62] Mattson MP. Excitotoxic and excitoprotective mechanisms: abundant targets for the prevention and treatment of neurodegenerative disorders. Neuromolecular Med 2003(3): 65- 94.
[63] Mattson MP. Metal-catalyzed disruption of membrane protein and lipid signaling in the pathogenesis of neurodegenerative disorder. Ann N Y Acad Sci 2004(1012): 37-50.
[64] Miura T, Suzuki K, Kohata N, Takeuchi H. Metal binding modes of Alzheimer's amyloid beta-peptide in insoluble aggregates and soluble complexes. Biochemistry 2000(39): 7024-7031.
[65] Narahashi T, Ma JY, Arakawa O, Reuveny E, and Nakahiro M. GABA receptor-channel complex as a target site of mercury, copper, zinc and lanthanides. Cell Mol Neurobiol 1994(14): 599-621.
[66] Niu ZD, Yu K, Gu Y, Wang M, She JQ, Chen WH, Ruan DY. Effects of copper on A-type potassium currents in acutely dissociated rat hippocampal CA1 neurons. Neuroreport 2005 (16): 1585-1589.
[67] Niu ZD, Wang M, Chen JT, Li XM, Ruan DY. Inhibition of delayed rectifier K~+ currents by copper in acutely dissociated rat hippocampal CA1 neurons. Toxicology Letters, accepted
[68] Nriagu JO ed. Copper in the environment: Part 1. Ecological cycling. New York, John Wiley & Sons Ltd, 1979b, PP43-75.
[69] O'Halloran TV, Culotta VC. Metallochaperones, an Intracellular Shuttle Service for Metal Ions. J Biol Chem 2000(275): 25057-2560.
[70] Owen CA Jr. Metabolism of radio copper (Cu~(64)) in the rat. Am J Physiol 1965(209): 900-904.
[71] Paris I, Dagnino-Subiabre A, Marcelain K, Bennett LB, Caviedes P, Caviedes R, Azar CO, Segura-Aguilar J. Copper neurotoxicity is dependent on dopamine-mediated copper uptake and one-electron reduction of aminochrome in a rat substantia nigra neuronal cell line. J Neurochem 2001(77): 519-529.
[72] Pena MM, Lee J, Thiele DJ. A delicate balance: homeostatic control of copper uptake and distribution. J Nutr 1999(129): 1251-1260.
[73] Pike CJ, Burdick D, Walencewicz AJ, Glabe CG, Cotman CW. Neurodegeneration induced by Neurodegeneration induced by beta-amyloid peptides in vitro: The role of peptide assembly state. J Neurosci 1993(13): 1676-1687.
[74] Reiser S, Smith JC, Mertz W, Holbrook JT, Scholfield DJ, Powell AS, Canfield WK, Canary JJ. Indices in copper status in humans consuming a typical American diet containing either fructose or starch. Am J Clin Nutr 1985(42):242-251.
[75] Robbins KR, Baker DH. Effect of sulfur amino acid level and source on the performance of chicks fed high levels of copper. Poult Sci 1980(59): 1246-1253.
[76] Sayre LM, Perry G, Atwood CS, Smith MA. The role of metals in neurodegenerative disease. Cell Mol Biol 2000(46): 731-741
[77] Sharonova IN, Vorobjev VS, Hass HL. High-affinity copper block of GABAa receptor-mediated currents in acutely isolated cerebellar Purkinje cells of the rat. Eur. J. Neurosci 1998(10): 522-528.
[78] Sharonova IN, Vorobjev VS, Haas HL. Interaction between copper and zinc at GABAa receptors in acutely isolated cerebellar Purkinje cells of the rat. Br J Pharmacol 2000(130): 851-856.
[79] Sliva JRRED, Williams RJP. The Biological Chemistry of the Elements: The Inorganic Chemistry of Life. Oxford: Clarendon Press, 1991.
[80] Soto F, Garcia-Guzman M, Gomez-Hernandez JM, Hollmann M, Karschin C, Stqhmer W. P2X4: an ATP-activated ionotropic receptor cloned from rat brain. Proc Natl Acad Sci USA 1996(93): 3684-3688.
[81] Sparks DL, Schreurs BCT. Trace amounts of copper in water induce β-amyloid plaques and learning deficits in a rabbit model of Alzheimer's disease. J Proc Natl Acad Sci 2003(100): 11065-11069.
[82] Squitti R, Cassetta E, Dal Forno G, Lupoi D, Lippolis G, Pauri F, Vernieri F, Cappa A, Rossini PM. Copper perturbation in 2 monozygotic twins discordant for degree of cognitive impairment. Arch Neurol 2004(61): 738-743.
[83] Sternlieb I. Copper and the liver. Gastroenterology 1980(78): 1615-1628.
[84] Strausak D, Mercer JF, Dieter HH, Stremmel W, Multhaup G. Copper in disorders with neurological symptoms: Alzheimer's, Menkes, and Wilson diseases. Brain Res Bull 2001 (55): 175-185.
[85] Szerdahelyi P, Kasa P. Variation in trace metal levels in rat hippocampus during ontogenetic development. Anat Embryol Berl 1983(167): 141-149.
[86] Szerdahelyi P, Kasa P. Histochemical demonstration of copper in normal rat brain and spinal cord. Evidence of localization in glial cells. Hischemistry 1986(85): 341-347.
[87] Tasaki M, Hanada K, Hashimoto I. Analyses of serum copper and zinc levels and copper/zinc ratios in skin diseases. J Dermatol 1993(20): 21-24.
[88] Thornalley PJ, Vasak M. Possible role for metallothionein in protection against radiation-induced oxidative stress. Kinetics and mechanism of its reaction with superoxide and hydroxyl radicals. Biochim Biophys Acta 1985(827): 36-44.
[89] Ting-Beall HP, Clark DA, Suelter CH, Wells WW. Studies on the interaction of chick brain microsomal (Na~+/ K~+)-ATPase with copper. Biochim Biophys Acta 1973(291): 229-236.
[90] Torsdottir G, Kristinsson J, Hreidarsson S, Snaedal J, Johannesson T. Copper, ceruloplasmin and superoxide dismutase (SOD1) in patients with Down's syndrome. Pharmacol Toxicol 2001(89): 320-325.
[91] Trombley PQ, Shepherd GM. Differential modulation by zinc and copper of amino acid receptors from rat olfactory bulb neurons. J. Neurophysiolo 1996(76): 2088-2094.
[92] Turnlund JR, Swanson CA, King JC. Copper absorption and retention in pregnant women fed diets based on animal and plant proteins. J Nutr 1983(113): 2346-2352.
[93] Turnlund JR. Copper. In: Shils M, Olson JA, Shike M, Ross AC, eds. Nutrition in Health and Disease. 9th ed. Baltimore: Williams & Wilkins; 1999:241-252.
[94] Van den Berg GJ, Beynen AC. Influence of ascorbic acid supplementation on copper metabolism in rats. Br J Nutr 1992(68): 701-715.
[95] VanLandingham JW, Fitch CA, Levenson CW. Zinc inhibits the nuclear translocation of the tumor suppressor protein p53 and protects cultured human neurons from copper induced neurotoxicity. Neuromolecular Med 2002(1): 171- 82.
[96] Varela-Nallar L, Toledo EM, Larrondo LF, Cabral AL, Martins VR, Inestrosa C. Induction of cellular prion protein (PrPC) gene expression by copper in neurons. Am J Physiol Cell Physiol 2006(290): 271-281.
[97] Vasic V, Jovanovic D, Krstic D, Nikezic G, Horvat A, Vujisic L, Nedeljkovic N. Prevention and recovery of CuSO_4induced inhibition of Na~+/K~+-ATPase and Mg~(2+)-ATPase in rat brain synaptosomes by EDTA. Toxicology Letters 110 (1999)95-104
[98] Virginio C, Church D, North RA, Surprenant A. Effects of divalent cations, protons and calmidazolium at the rat P2X_7 receptor. Neuropharmacology 1997(36): 1285-1294.
[99] Vlachova V, Zemkova H, Vyklicky L Jr. Copper modulation of NMDA responses in mouse and rat cultured hippocampal neurons. Eur J Neurosci 1996(8): 2257-2264.
[100] Waggoner DJ, Bartnikas TB, Gitlin JD. The role of copper in neurodegenerative disease. Neurobiol Dis 1999(6): 221-230.
[101] Waggoner DJ, Drisaldi B, Bartnikas TB, Casareno RL, Prohaska JR, Gitlin JD, Harris DA. Brain copper content and cuproenzyme activity do not vary with prion protein expression level. J Biol Chem 2000(275): 7455-7458.
[102] Wang DS, Zhu HL, Hong Z, Li JS. Cu~(2+) inhibition of glycine-activated currents in rat sacral dorsal commissural neurons. Neurosci Lett 2002(328): 117-120.
[103] 王刚 黄振信 祝延，《钾通道功能异常与阿尔茨海默病》。国外医学，老年医学分册 2002(23)：230-232．
[104] 王海鹏，于晓军，何欣，铜与机体防御功能。微量元素与健康研究 2004(21)：58-61
[105] Wang KT. Cu~(2+)induces Ca~(2+)-dependent neurotransmitter release from brain catecholaminergic nerve terminals. Eur J of Pharmacol. 1999(373): 163-169.
[106] 王夔，生命科学中的微量元素[M]。中国计量出版社，1996。
[107] Wapnir RA, Balkman C. Intestinal absorption of copper: influence of carbohydrates. Biochem Med Metab Biol 1992(47): 47-53.
[108] Weiser T, Wienrich M. The effects of copper ions on glutamate receptors in cultured rat cortical neurons. Brain Res. 1996(742): 211-218.
[109] Klein WL, Krafft GA, Finch CE. Targeting small Aβ oligomers: the solution to an Alzheimer's disease conundrum? Trends in Neurosci 2001 (24): 219-224.
[110] Wong BS, Brown DR, Sy MS. A Yin-Yang role for metals in prion disease. Panminerva Med 2001(43): 283-7.
[111] Wong PY, Fritze K. Determination by neutron activation of copper, manganese, and zinc in the pineal body and other areas of brain tissue. J Neurochem 1969; 16: 1231-1234.
[112] 吴茂江，涂长信，微量元素与健康研究。铜与人体健康2005(22)：64-65。
[113] Xie X, Hider RC, Smart TG. Modulation of GABA-mediated synaptic transmission by endogenous zinc in the immature rat hippocampus in vitro. J Physiol (Lond) 1994(478): 75-86.
[114] Xie X, Smart TG. Modulation of long-term potentiation in rat hippocampal pyramidal neurons by zinc. Pfluegers Arch 1994(427): 481-486.
[115] Xiong K, Peoples RW, Montgomery JP, Chiang Y, Stewart RR, Weight FF, Li C. Differential modulation by copper and zinc of P2X2 and P2X4 receptor function. J Neurophysiol 1999(81): 2088-2094.
[116] Yakushiji T, Tokutomi N, Akaike N, Carpenter DO: Antagonists of GABA responses, studied using internally perfused frog dorsal root ganglion neurons. Neuroscience 1987(22): 1123-1133.
[117] Ye CP, Selkoe DJ, Hartley DM. Protofibrils of amyloid beta-protein inhibit specific K~+ currents in neocortical cultures. Neurobiol Dis 2003(13): 177-190.
[1] Alkon DL. Calcium-mediated reduction of ionic currents: A biophysical memory trace. Science 1994(226): 1037-1045.
[2] Alshuaib WB, Mathew MV. Inhibition of transient K~+ current by copper in Drosophila neurons. Neurochem Res 2004(29): 785-789.
[3] Atwood CS, Huang X, Moir RD, Tanzi RE, Bush AI. Role of free radicals and metal ions in the pathogenesis of Alzheimer's disease. Met Ions Biol Syst 1999(36): 309-364.
[4] Atwood CS, Moir RD, Huang X, Scarpa RC, Bacarra ME, Romano DM, Hartshorn MA, Tanzi RE, Bush AI. Dramatic aggregation of Alzheimer abeta by Cu(II) is induced by conditions representing physiological acidosis. J Biol Chem 1998(273): 12817-12826.
[5] Bardoni R, Beluzzi O. Kinetic study and numerical reconstruction of A-type current in granule cells of rat cerebellar slices. J Neurophysiol 1993(69): 222-223.
[6] Brewer GJ. Yusbasian-Gurkan, V. Wilson's disease. Medicine 1992(71): 139-164.
[7] Bush AI. Metals and neuroscience. Curr Opin Chem Biol 2000(4): 184-191.
[8] Chu Chen. β-Amyloid increases dendritic Ca~(2+) influx by inhibiting the A-type K~+ current in hippocampal CA1 pyramidal neurons. Biochemical and Biophysical Research Communications 2005(338): 1913-1919.
[9] Cowan TM, Siegel RW. Drosophila mutations that alter ionic conduction disrupt acquisition and retention of a conditioned odor avoidance response. J. Neurogenet 1986(3): 187-201.
[10] Crow T. Cellular and molecular analysis of associative learning and memory in Hermissenda. Trends Neurosci 1988(11): 136-142.
[11] Debanne D, Guerineau NC,, Gahwiler BH, Thompson SM. Action-potential propagation gated by an axonal I_A-like K~+ conductance in hippocampus. Nature 1997(389): 286-289.
[12] Dedek K, Kunath B, Kananura C, Reuner U, Jentsch TJ, Steinlein OK. Myokymia and neonatal epilepsy caused by a mutation in the voltage sensor of the KCNQ2 K~+ channel. Proc Natl Acad Sci USA. 2001(98): 12272-12277.
[13] Dodart JC, Bales KR, Gannon KS, Greene SJ, DeMattos RB, Mathis C, DeLong CA, Wu S, Wu X, Holtzman DM, Paul SM. Immunization reverses memory deficits without reducing brain Aβ burden in Alzheimer's disease model. Nat Neurosci 2002(5): 452-457.
[14] Fraser SP, Suh YH, Djamgoz MBA. Ionic effects of the Alzheimer's disease β-amyloid precursor protein and its metabolic fragments. Trends Neurosci 1997(20): 67-72.
[15] Giese KP, Storm JF, Reuter D, Fedorov NB, Shao LR, Leicher T, Pongs O, Silva AJ. Reduced K~+ channel inactivation, spike broadening, and after- hyperpolarization in Kvbeta 1.1-deficient mice with impaired learning. Learn Mem. 1998(5): 257-73.
[16] Good TA, Smith DO and Murphy RM. β-Amyloid peptide blocks the fast-inactivating K~+ current in rat hippocampal neurons. Biophys J 1996(70): 296-304.
[17] Hamill, O.P., Marty, A., Neher, E., Sakmann, B., Sigworth, F.J., Improved patch-clamp techniques of high-resolution current recording from cells and cell-free membrane patchs. Pfluegers. Arch. 1981(391): 85-100.
[18] Hardy JA, Higgins GA. Alzheimer's disease: The amyloid cascade hypothesis. Science 1996(256): 184-185.
[19] Hartter D, Barnea A. Evidence for release of copper in the brain: depolarization- induced release of newly taken-up 67copper. Synapse 1988(2): 412-415.
[20] Hartley D, Walsh DM, Ye CP, Diehl T, Vasquez S, Vassilev PM, Teplow DB, Selkoe DJ. Protofibrillar intermediates of amyloid β-protein induce acute electrophysiological changes and progressive neurotoxicity in cortical neurons. J Neurosci 1999(19): 8876-8884.
[21] Hoffman DA, Magee JC, Colbert CM, Johnston D. K~+ channel regulation of signal propagation in dendrites of hippocampal pyramidal neurons. Nature 1997(387): 869-875.
[22] Horning MS, Trombley PQ. Zinc and copper influence excitability of rat olfactory bulb neurons by multiple mechanisms. J Neurophysiol 2001(86): 1652-1660.
[23] Huang X, Cuajungco MP, Atwood CS, Hartshorn MA, Tyndall JD, Hanson GR, Stokes KC, Leopold M, Multhaup G, Goldstein LE, Scarpa RC, Saunders AJ, Lim J, Moir RD, Glabe C, Bowden EF, Masters CL, Fairlie DP, Tanzi RE, Bush AI. Cu(II) potentiation of alzheimer abeta neurotoxicity. Correlation with cell-free hydrogen peroxide production and metal reduction. J Biol Chem 1999 (274): 3111-37116.
[24] Kaczmarek LK. Voltage-dependent potassium channels: minK and Shaker families. New Biol 1991(3): 315-323.
[25] Kaneda M, Nakamura H, Akaike N. Mechanism and enzymatic isolation of mammalian CNS neurons. Neurosci. Res. 1988(5): 299-315.
[26] Kardos J, Kovacs I, Hajos F, Kalman M, Simonyi M. Nerve endings from rat brain tissue release copper upon depolarization. A possible role in regulating neuronal excitability. Neurosci Lett 1989(103): 139-144.
[27] Kubisch C, Schroeder BC, Friedrich T, Lutjohann B, El-Amraoui A, Marlin S, Petit C, Jentsch TJ. KCNQ4, a novel potassium channel expressed in sensory outer hair cells, is mutated in dominant deafness. Cell 1999(5): 437-446.
[28] Lambert MP, Barlow AK, Chromy BA, Edwards C, Freed R, iosatos M, Morgan TE, Rozovsky I, Trommer B, Viola KL, Wals P, Zhang C, Finch CE, Kraff, GA, Klein WL, Diffusible, nonfribrillar ligands derived from Aβ1-42 are potent central nervous system neurotoxins. Proc Natl Acad Sci USA 1998(95): 6448-6453.
[29] LeMasson G, Marder E, Abbott LF. Activity-dependent regulation of conductances in model neurons. Science 1993(259): 1915-1917.
[30] Lorenzo A, Yankner BA. β-Amyloid neurotoxicity requires fibril formation and is inhibited by Congo red. Proc Natl Acad Sci USA 1994(91): 12243-12247.
[31] Lovell M A, Robertson J D, Teesdale W J, Campbell J L, Markesbery WR. Copper, iron and zinc in Alzheimer's disease senile plaques. J Neurol Sci 1998(158): 47-52.
[32] Lutsenko S, Petris MJ. Function and regulation of the mammalian copper-transporting ATPases: insights from biochemical and cell biological approaches. J Membr Biol 2003(191): 1-12.
[33] Ma M, J Koester. The role of K~+ currents in frequency-dependent spike broadening in Aplysia R20 neurons: A dynamic-clamp analysis. J Neurosci 1996(16): 4089-4101.
[34] Maynard CJ, Cappai R, Volitakis I, Cherny RA, White AR, Beyreuther K, Masters CL, Bush AI, Li QX. Overexpression of Alzheimer's disease amyloid-beta opposes the age-dependent elevations of brain copper and iron. J Biol Chem. 2002(277):44670-44676.
[35] Murase K, Ryu PD, Randic M. Excitatory and inhibitory amino acids and peptide-induced responses in acutely isolated rat spinal dorsal horn neurons. Neurosci Lett. 1989(103): 56-63.
[36] Okeda R, Gei S, Chen I, Okaniwa M, Shinomiya M, Matsubara O, Menkes' kinky hair disease: morphological and immunohistochemical comparison of two autopsied patients. Acta Neuropathol (Berl) 1991(81): 450-457.
[37] Pike CJ, Burdick D, Walencewicz AJ, Glabe CG, Cotman CW. Neurodegeneration induced by Neurodegeneration induced by β-amyloid peptides in vitro: The role of peptide assembly state. J Neurosci 1993(13): 1676-1687.
[38] Roeper J, O Pongs. Presynaptic potassium channels. Curr Opin Neurobiol 1996(6): 338-341.
[39] Rudy B. Diversity and ubiquity of K channels. Neurosci 1988(25): 729-749.
[40] Shirasaki T, Klee MR, Nakaye T, Akaike N. Differential blockade of bicuculline and strychnine on GABA- and glycine-induced responses in dissociated rat hippocampal pyramidal cells. Brain Res. 1991(561): 77-83.
[41] Southan AP, Robertson BJ. Patch-clamp recordings from cerebellar basket cell bodies and their presynaptic terminals reveal an asymmetric distribution of voltage-gated potassium channels. Neurosci 1998(18): 948-955.
[41] Sparks DL, Schreurs BG. Trace amounts of copper in water induce P-amyloid plaques and learning deficits in a rabbit model of Alzheimer's disease. Proc Natl Acad Sci USA 2003(100): 11065-11069.
[42] Storm JF. Action potential repolarization and a fast fter-hyperpolarization in rat hippocampal pyramidal cells. J Physiol (Lond) 1987(385): 733-759.
[43] Szerdahelyi P, Kasa P. Variation in trace metal levels in rat hippocampus during ontogenetic development. Anat Embryol Berl 1983(167):141-149.
[44] Szerdahelyi P, Kasa P. Histochemical demonstration of copper in normal rat brain and spinal cord. Evidence of localization in glial cells. Hischemistry 1986(85): 341-347.
[45] Wang HW, Pasternak JF, Kuo H, Ristic H, Lambert MP, Chromy B, Viola KL, Klein WL, Stine WB, Krafft GA, Trommer BL, Soluble oligomers of beta amyloid (1-42) inhibit long-term potentiation but not long-term depression in rat dentate gyrus. Brain Res 2002(924): 133-140.
[46] Wong PY, Fritze K. Determination by neutron activation of copper, manganese, and zinc in the pineal body and other areas of brain tissue. J Neurochem 1969(16): 1231-1234.
[1] Alshuaib WB, Mathew MV. Inhibition of transient K~+ current by copper in Drosophila neurons. Neurochem Res 2004(29) 785-789.
[2] Arhem P. Effects of some heavy metal ions on the ionic currents of myelinated fibres from Xenopus laevis. J. Physiol London 1980(306): 219-231.
[3] Assaf SY, Chung SH, Release of endogenous Zn~(2+) from brain tissue during activity. Nature 1984(308): 734-736.
[4] Bayer TA, Schafer S, Simons A, Kemmling A, Kamer T, Tepest R, Eckert A, Schussel K, Eikenberg O, Sturchler-Pierrat C, Abramowski D, Staufenbiel M, Multhaup G, Dietary Cu stabilizes brain superoxide dismutase 1 activity and reduces amyloid Aβ production in APP23 transgenic mice Proc Natl Acad Sci USA 2003(100): 14187-14192.
[5] Beckman JS. Peroxynitrite versus hydroxyl radical: the role of nitric oxide in superoxide-dependent cerebral injury. Ann N Y Acad Sci 1994(738): 382-387.
[6] Brewer GJ, Yusbasian-Gurkan V. Wilson's disease. Medicine 1992(71): 139-164.
[7] Brown DR. Copper and prion disease. Brain Res Bull 2001(55): 165-173.
[8] Bull PC, Cox DW. Wilson disease and Menkes disease: new handles on heavy-metal transport. Trends Genet. 1994(10): 246-252.
[9] Coddou C, Moralesl B, Huidobro-Toro JP. Neuromodulator role of zinc and copper during prolonged ATP applications to P2X_4 purinoceptors. Eur. J. Pharmacol. 2003(472): 49- 56.
[10] Hamill, OP, Marty A, Neher E, Sakmann B, Sigworth FJ. Improved patch-clamp techniques of high-resolution current recording from cells and cell-free membrane patchs. Pfluegers. Arch. 1981(391): 85-100.
[11] Saito T, Okabe M, Hosokawa T, Kurasaki M, Hata A, Endo F, Nagano K, Matsuda I, Urakami K, Saito K. Immunohistochemical determination of the Wilson Coppertransporting P-type ATPase in the brain tissues of the rat. Neurosci. Lett. 1999(266): 13-16.
[12] Horning MS, Trombley PQ. Zinc and copper influence excitability of rat olfactory bulb neurons by multiple mechanisms. J. Neurophysiol. 2001(86): 1652-1660.
[13] Hui K, Davis BA, Boulton AA. Analysis of copper in brain by the masspectrometric-integrated-ion-current procedure. Neurochem. Res. 1987(2): 495-506.
[14] Kaneda M, Nakamura H, Akaike N. Mechanism and enzymatic isolation of mammalian CNS neurons. Neurosci. Res. 1988(5): 299-315.
[15] Kardos J, Kovacs I, Hajos F, Kalman M, Simonyi M. Nerve endings from rat brain tissue release copper upon depolarization. A possible role in regulating neuronal excitability. Neurosci. Lett. 1989(103): 139-144.
[16] Kim H, Macdonald RL. An N-terminal histidine is the primary determinant of a subunit-dependent Cu~(2+) sensitivity of αβ3γ2L GABAa receptors. Mol. Pharmacol. 2003(64): 1145-1152.
[17] Kues WA, Wunder F. Heterogeneous expression patterns of mammalian potassium channel genes in developing and adult rat brain. Eur. J. Neurosci. 1992(4):1296-1308.
[18] LeMasson G, Marder E, Abbott LF. Activity-dependent regulation of conductances in model neurons. Science. 1993(259): 1915-1917.
[19] Li C, Peoples RW, Weight FF. Cu~(2+) potently enhances ATP-activated current in rat nodose ganglion neurons. Neurosci. Lett. 1996(219): 45-48.
[20] Lutsenko S, Cooper MJ. Localization of the Wilson's disease protein product to mitochondria. Proc. Natl. Acad. Sci. U. S. A. 1998(95): 6004-6009.
[21] Nalbandyan RM. Copper in brain. Neurochem. Res. 1983(8):1211-1232.
[22] Niu ZD, Yu K, Gu Y, Wang M, She JQ, Chen WH, Ruan DY. Effects of copper on A-type potassium currents in acutely dissociated rat hippocampal CA1 neurons. Neuroreport, 2005(16): 1585-1589.
[23] Okeda R, Gei S, Chen I, Okaniwa M, Shinomiya M, Matsubara O. Menkes' kinky hair disease: morphological and immunohistochemical comparison of two autopsied patients. Acta Neuropathol. Berl. 1991(81): 450-457.
[24] Olivares M, Uauy R. Copper as an essential nutrient. Am. J. Clin. Nutr. 1996(63): (Suppl.), 791S-796S.
[25] Phinney AL, Drisaldi B, Schmidt SD, Lugowski S, Coronado V, Liang Y, Home P, Yang J, Sekoulidis J, Coomaraswamy J, Chishti MA, Cox DW, Mathews PM, Nixon RA, Carlson GA, St George-Hyslop P, Westaway D. In vivo reduction of amyloid-β by a mutant copper transporter, Proc. Natl. Acad. Sci. U.S.A. 2003(100): 14193-14198.
[26] Saito T, Okabe M, Hosokawa T, Kurasaki M, Hata A, Endo F, Nagano K, Matsuda I, Urakami K, Saito K. Immunohistochemical determination of the Wilson Copper transporting P-type ATPase in the brain tissues of the rat. Neurosci Lett. 1999(266): 13-16.
[27] Scheinberg IH, Sternlieb I. Wilson's disease. In: Smith LH Jr, editor. Major problems in internal medicine 1984(23): Philadelphia: WB Saunders Co.
[28] Sharonova IN, Vorobjev VS, Hass HL. High-affinity copper block of GABA_A receptor-mediated currents in acutely isolated cerebellar Purkinje cells of the rat. Eur. J. Neurosci. 1998(10): 522-528.
[29] Sheline CT, Choi EH, Kim-Han JS, Dugan LL, Choi DW. Cofactors of mitochondrial enzymes attenuate copper-induced death in vitro and in vivo. Ann. Neurol. 2002(52): 195-204.
[30] Simonian NA, Coyle JT. Oxidative stress in neurodegenerative diseases. Annu. Rev. Pharmacol. Toxicol. 1996(36): 83-106.
[31] Sorenson RJ. Prion diseases: copper deficiency states associated with impaired nitrogen monoxide or carbon monoxide transduction and translocation. J.Inorg. Biochem. 2001 ( 87): 125-127.
[32] Sparks DL, Schreurs BG. Trace amounts of copper in water induce β-amyloid plaques and learning deficits in a rabbit model of Alzheimer's disease. Proc. Natl. Acad. Sci. U.S.A. 2003(100): 11065-11069.
[33] Trombley PQ, Shepherd GM. Differential modulation by zinc and copper of amino acid receptors from rat olfactory bulb neurons. J. Neurophysiolo. 1996(76): 2088-2094.
[34] Vlachova V, Zemkova H, Vyklicky LJr. Copper modulation of NMD A responses in mouse and rat cultured hippocampal neurons. Eur. J. Neurosci. 1996(8): 2257-2264.
[35] Wang DS, Zhu HL, Hong Z, Li JS. Cu~(2+) inhibition of glycine-activated currents in rat sacral dorsal commissural neurons. Neurosci Lett. 2002(328): 117-120.
[36] Wang KT. Cu~(2+) induces Ca~(2+)-dependent neurotransmitter release from brain catecholaminergic nerve terminals. European J of Pharmacology. 1999(373): 163-169.
[37] Weiser T, Wienrich M. The effects of copper ions on glutamate receptors in cultured rat cortical neurons. Brain Res. 1996(742): 211-218.
[38] Yost CS. Potassium channels: basic aspects, functional roles, and medical significance, Anesthesiology. 1999(90): 1186-1203.