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研究生:黃民瑋
研究生(外文):Ming-Wai Huang
論文名稱:霍奇金-赫胥黎模型中的自律現象
論文名稱(外文):Spontaneous Oscillations in Hodgkin-Huxley Model
指導教授:洪 子 倫
指導教授(外文):Tzyy-Leng Horng
學位類別:碩士
校院名稱:逢甲大學
系所名稱:應用數學所
學門:數學及統計學門
學類:數學學類
論文種類:學術論文
論文出版年:2006
畢業學年度:94
語文別:英文
論文頁數:25
中文關鍵詞:霍奇金-赫胥黎模型分歧分析鈉離子通道鉀離子通道細胞外鉀離子濃度
外文關鍵詞:sodium channelbifurcation analysisHodgkin-Huxley modelpotassium channelextracellular potassium concentration
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神經元自發火現象是個在神經科學上重要且有趣的現象。本文藉著研究霍奇金-赫胥黎模型之分歧分析發現提高鈉離子通道之最大電導,或降低鉀離子通道之最大電導,或提高細胞外鉀離子濃度均可發生自發性振動,意即使得神經元產生自律性。提高細胞外鉀離子濃度會導致神經元自發火現象業已由實驗證實且為一普為人知的現象。但改變離子通道之最大電導,亦即改變離子通道之通透性,亦可導致神經元自發火現象則尚未經實驗證實。吾人希望未來的實驗可以驗證本文之發現。
Automatic neuron firing is an important and interesting research subject in neuroelectrophysiology. Through the original Hodgkin-Huxley model, we investigate its codimension 1 bifurcations along maximum conductance of sodium channel, maximum conductance of potassium channel, and extracellular potassium concentration. We find that increasing maximum conductance of sodium channel, or decreasing maximum conductance of potassium channel, or increasing extracellular potassium concentration will all cause spontaneous oscillation without any external stimulus current. The effect that increasing extracellular potassium concentration will cause repetitive neuron firing has been verified by experiments, but the effect of changing channel maximum conductance will cause automatic neuron firing is first analyzed in the current paper but not yet verified by experiments. We hope the experiment can be done in the future by using sodium channel activator and potassium channel blocker.
Contents

1. Introduction ……………………………………………...1

2. Mathematical Model and Numerical Method………….3

3. Results and Discussions……………………………….....6
3.1 Bifurcation along maximum conductance of sodium channel………………………………….....6
3.2 Bifurcation along maximum conductance of potassium channel……………………………..…10
3.3 Bifurcation along extracelluar potassium concentration ………………………………….....13

4. Conclusions……………………………………………..17

References………………………………………………18
[1] Hodgkin AL and Huxley AF, A Quantitative Description of Membrane Current and its Application to Conduction and Excitation in Nerve, 1952, J. Physiol, 117:500-544.
[2] Guevara MR, Bifurcations Involving Fixed Points and Limit Cycles in Biological Systems, In: “Nonlinear Dynamics in Physiology and Medicine”, edited by Beuter A, Glass L, Mackey MC, Titcombe MS, Springer-Verlag, New York, pp. 41-85 (2003).
[3] Borisyuk A and Rinzel J, Understanding neuronal dynamics by geometrical dissection of minimal models, In: “Models and Methods in Neurophysics”, edited by Chow C, Gutkin B, Hansel D, Meunier C, Dalibard J, Proc Les Houches Summer School 2003, (Session LXXX), Elsevier, pp. 19-72 (2005).
[4] Guckenheimer J and Oliva RA, Chaos in the Hodgkin–Huxley Model, 2002 SIADS, 1:105-114.
[5] Fukai H, Nomura T, Doi S, Sato S, Hopf bifurcations in multiple-parameter space of the hodgkin-huxley equations II. Singularity theoretic approach and highly degenerate bifurcations, 2000, Biol. Cybern., 82(3):223-9.
[6] Izhikevich EM, Neural Excitability, Spiking, and Bursting, 2000, Int. J. Bif. Chaos, 10:1171-1266.
[7] FitzHugh R, Theoretical effect of temperature on threshold in the Hodgkin-Huxley nerve model, 1966, J. Gen. Physiol., 49: 989-1005.
[8] Guttman RS and Barnhill R, Oscillation and repetitive firing in squid axons, 1970, J. Gen. Physiol., 55:104–118.
[9] Feudel U, Neiman A, Pei X, Wojtenek W, Braun HA, Huber MT, Moss F, Homoclinic bifurcations in a Hodgkin-Huxley model of thermally sensitive neurons, 2000, Chaos 10: 231-239.
[10] K. Aihara and G. Matsumoto , Two Stable Steady States In the Hodgkin-Huxley Axon,
[11] P. J. Hahn and D. M. Durand , Bistability Dynamics in Simulations of Neural Activity in High-Extracellular-Potassium Conditions, Journal of Computational Neuroscience 11, 5–18, 2001
[12] Schmid G, Goychuk I, Hanggi P, Effect of channel block on the spiking activity of excitable membranes in a stochastic Hodgkin-Huxley model, 2004, Phys Biol., 1(1-2):61-6.
[13] Ermentrout B, Simulating, Analyzing, and Animating Dynamical Systems: A Guide to XPPAUT for Researchers and Students, SIAM, Philadelphia, 2002.
[14] Dargent B and Couraud F, Down-regulation of voltage-dependent sodium channels initiated by sodium influx in developing neurons, Proc. Nati. Acad. Sci. USA, 1990, 87:5907-5911.
[15] Massensini AR, Romano-Silva MA, Gomez MV, Sodium Channel Toxins and Neurotransmitter Release, Neurochemical Research, 2003, 28(10):1607–1611.
[16] Lenaeus MJ, Vamvouka M, Focia PJ, Gross A, Structural basis of TEA blockade in a model potassium channel, Nat. Struct. Mol. Biol., 2005, 12(5):454-9.
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